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Written by Dr. Muhammad Dalmau   

CONTENTS

Introduction
I. The current definition of HIV-AIDS 4

II. Epidemiological approach to the HIV-AIDS theory 10

III. Morphogenesis of the HIV-AIDS theory 16

IV. Analysis of the evidence of the HIV-AIDS phenomenon 23

V. Deconstruction of the apparent paradox 68

VI. The long-run economic cost of AIDS-budgets 76

VII. Conclusions 77

References 90


INTRODUCTION

The first descriptions of AIDS cases in the scientific literature are from the early 1980s.
They suggest a possible acquired immune deficiency as the underlying factor responsible
for the increase of particular recurring diseases among very marginal groups of people in
certain American conurbations such as New York, San Francisco and Los Angeles.
All the members of these particular risk groups were identified as having healthhazardous
lifestyles. The diseases were exclusively limited to the behavioural risk groups.
Acquired immune deficiency syndrome, as the USA’s Centres for Disease Control
(CDC) named it in 1981, was identified as a possible behavioural disease.
Up until 1983, AIDS was a disease relegated to big cities in the USA and Europe. In
April 1984 it was announced that a newly discovered virus, HIV, was the cause of
AIDS. Since then the world has lived under the threat of this permanent epidemic of
potentially lethal consequences.
I have been asked by a group of concerned South African Muslims about the nature of
AIDS and the bleak prospect of the AIDS epidemic in the African continent. In the
media we see a constant update of the figures associated with AIDS. Apocalyptic
estimates from different international health agencies predict a catastrophic future.

I. THE CURRENT DEFINITION OF HIV-AIDS

The acronyms HIV and AIDS mean respectively ‘Human Immune-deficiency Virus’ and
‘Acquired Immune Deficiency Syndrome’. HIV is attached to AIDS, as in ‘HIV-AIDS’,
to indicate that HIV is the cause of AIDS.
In any current medical text book we find that HIV-AIDS comes under the category of
‘Sexually Transmitted Diseases’ (STDs).(131)

Epidemiology

Acquired Immune Deficiency Syndrome was first described as a clinical entity in 1981,
and HIV was identified as the causative organism in 1983. In December 1997 the World
Health Organisation (WHO) estimated that 29 million adults and 1.5 million children
were already infected, and that up to 16,000 new infections occur daily world-wide. The
WHO long-term projections estimated a cumulative total of over 40 million infections by
the year 2000.
HIV is predominantly concentrated in developing countries among people in early adult
life. Although HIV can be isolated from a wide range of body fluids and tissues, the
majority of infections are considered to be transmitted via semen, cervical secretions and
blood.

The cause

HIV is considered to be the cause of AIDS. HIV is a lentivirus (slow-virus) of the family
of retroviruses. There are at least two types, HIV-1 and HIV-2. HIV-2 is almost
confined to West Africa although there is evidence of some spread to the Indian
subcontinent. It is associated with an AIDS-type illness.
Retroviruses are characterised by possessing the enzyme Reverse Transcriptase, which
allows viral RNA to be transcribed into DNA, and hence incorporated into the host cell
genome (the DNA of the cell infected by the virus). Reverse transcription is a highly
error-prone process with a significant rate of mis-incorporation of bases (wrong
assembly of DNA bases). This, combined with the high rate of viral turnover, leads to
considerable genetic variation and a diversity of viral subtypes.
5

Transmission

a) Sexual intercourse
World-wide, heterosexual intercourse accounts for the vast majority of infections, and
co-existent sexually transmitted diseases, especially those causing genital ulceration,
enhance transmission. The passage of HIV appears to be more efficient from men to
women, and from men to the passive partner in anal intercourse, than vice versa.
Homosexual transmission still accounts for the majority of infections in the USA and
Europe, but there appears to be an increasing rate of heterosexual transmission in
developed countries. Up to 18% of infections in Europe are thought to be heterosexually
acquired.
In central and sub-Saharan Africa the epidemic has always been heterosexual, and more
than half the infected adults in these regions are women.
South East Asia and the Indian subcontinent are still in the early phases of a possible
explosive epidemic, driven by promiscuous heterosexual intercourse and a high incidence
of other sexually transmitted diseases.
b) Mother-to-child transmission
Vertical transmission is the most common route of HIV infection in children. European
studies suggest that 15% of babies born to HIV-infected mothers are likely to develop
AIDS, in the USA and Africa the rates of mother-to-child transmission are up to 40%.
Breast-feeding has been shown to increase the risk of vertical transmission by up to 20%.
Vertical transmission can be reduced by the use of zidovudine (AZT) and the numbers of
infected children have fallen in areas where zidovudine is used.
c) Contaminated blood, blood products and organ donations
Screening of blood and blood products was introduced in 1985 in Europe and the USA.
Prior to this, HIV infection was associated with the use of clotting factors for
haemophilia and with blood transfusions.
The practice of sharing needles and syringes for intravenous drug misuse continues to be
a major route of transmission of HIV in Europe, USA, South East Asia and Latin
America. Health care workers have a risk of approximately 0.3% following a single
needle stick injury with known HIV infected blood.
6

Pathogenesis

HIV attacks the immune system of the host. HIV recognises the CD4+ molecule in the
surface of T4 lymphocytes. By interaction with this molecule, HIV enters the T4-cell.
After transferring the viral genetic material into the cell DNA, it uses the cell machinery
to produce its own viral particles, and finally destroys the T4-cell. Studies of viral
turnover in HIV-positive individuals have demonstrated a virus half-life in the circulation
of about six hours. Virus production by infected cells lasts for about two days and is
probably limited by the death of the cell owing to direct HIV effects, linking HIV
replication to the process of CD4+ destruction and depletion. Cell mediated
(macrophage) immune deficiency is the major consequence leaving the host open to
infections with intracellular pathogens, whilst the coexisting antibody abnormalities
(decrease of T4-cells) predispose to infections with capsulated bacteria.

Diagnosis

HIV infection is diagnosed either by detection of virus-specific antibodies (anti-HIV) or
by direct identification of the viral material. These antibodies have no protective function
and some of them persist for life, like IgG gp120, except in babies from HIV infected
mothers, where they are lost gradually over the first 18 months of life.
Other antibodies like IgG p24 disappear as the disease progresses.
Viral p24 antigen (p24ag) is detectable shortly after the infection but has usually
disappeared by 8-10 weeks after exposure.

Laboratory

The blood abnormalities include lymphopenia (low count of lymphocytes) with atypical
reactive lymphocytes, thrombocytopenia (low count of platelets) and raised liver
enzymes. CD4+ lymphocytes may be markedly depleted and the CD4+/CD8+ ratio
reversed.
Antibodies to HIV may be absent during the early stage of infection although the level of
circulating RNA is high and p24 core protein may be detectable.
7

Clinical latency

The majority of people with HIV infection (HIV-positive test) are asymptomatic for a
substantial but variable length of time. However, the virus continues to replicate and the
person is infectious. Studies suggest a median time of 10 years from infection to
development of AIDS, although some patients progress rapidly and others remain
symptom-free for up to 20 years.
Gender and pregnancy per se do not appear to influence the rate of progression.

Clinical features of HIV infection

The spectrum of illnesses associated with HIV infection is broad, and is the result of both
direct HIV effects and the associated immune dysfunction. The classification depends to
a large extent on definitive diagnoses of infection, which makes it more difficult to use in
those areas of the world without sophisticated laboratory support. As immunesuppression
progresses, the patient is susceptible to an increasing range of opportunistic
infections and tumours.
There are 29 diseases included in this syndrome, none of which is new, meaning that
most of them have well-known causes other than HIV, like funguses, bacteria,
mycobacterium, and viruses. Still others, like various cancers and neoplasms, have no
established aetiology, and others like dementia or wasting syndrome have on their own
many different causes. All of the following diseases are classified as AIDS-indicator
diseases when there is a positive HIV-test:
1) Bacterial infections, multiple or recurrent (applies only to children)
2) Candidiasis of bronchia, trachea or lungs
3) Candidiasis of oesophagus
4) CD4+ T-lymphocyte count <200 cells/microliter (or a CD4+ percentage <14)
5) Cervical cancer, invasive
6) Coccidioidomycosis, disseminated or extra-pulmonary
7) Cryptococcosis, extra-pulmonary
8) Cryptococcosis, chronic intestinal
9) Cytomagalovirus disease other than retinitis
10) Cytomegalovirus retinitis
11) HIV encephalopathy (dementia)
12) Herpes simplex, with esophagitis, pneumonia, or chronic mucocutaneous ulcers
13) Histoplasmosis, disseminated or extra-pulmonary
14) Isosporiasis, chronic intestinal
8
15) Kaposi’s sarcoma
16) Leukoencephalopathy, progressive multifocal
17) Lymphoid interstitial pneumonia and/or pulmonary lymphoid hyperplasia
18) Lymphoma, Burkitt’s
19) Lymphoma, immunoblastic
20) Lymphoma, primary in brain
21) Mycobacterium avium or mycobacterium kansasii, disseminated or extra-pulmonary
22) Mycobacterium tuberculosis, disseminated or extra-pulmonary
23) Mycobacterial diseases, other disseminated or extra-pulmonary
24) Pneumocystis carinii pneumonia
25) Pneumonia, recurrent (within a 12-month period)
26) Salmonella septicaemia, recurrent
27) Toxoplasmosis of the brain
28) Tuberculosis, pulmonary
29) Wasting syndrome, HIV
Numbers 3, 4, 10, 15, 17, 21-25 and 27-29 are considered ‘definitive diagnoses’ or
‘presumptive diagnoses’.
In Africa the clinical indication with or without a positive HIV test is: fever for more
than two months + diarrhoea for more than two months + loss of body weight of more
than 10% + persistent cough.

Treatment

Despite the introduction of new anti-retroviral drugs there is still no cure for HIV and
AIDS, so the patient must live with a chronic, progressive, infectious and unpredictable
condition.
The principal aim of anti-retroviral drug therapy is to suppress viral replication to as low
a level as possible for as long as possible, in order to delay the progression of the disease.
The evidence shows more benefits from anti-retrovirals used in combination. However,
none of the present combinations eradicate HIV. Inhibitors of HIV-reverse transcriptase
and of HIV-protease are so far the most developed.
The scientific rationale for early intervention—the ‘hit early and hit hard’ philosophy—is
based on the rapid turnover that has been demonstrated throughout all stages of
infection, and the view that the earlier and the more thoroughly viral replication is
9
suppressed, the less likely the immune system is to be damaged and the virus to develop
resistance. Treatment is initiated at least with two or three drugs. The potential for
adverse reactions and drug interactions is greater with more drugs.
However, it must be remembered that HIV has a long period of clinical latency despite
continuing viral activity. None of the current therapeutic regimens is likely to be able to
eradicate the virus from an individual, and there is a lack of data on the long-term
effectiveness and toxicity of anti-retrovirals.
During pregnancy, HIV-positive mothers are treated with AZT to treat or prevent the
development of AIDS, and also to reduce the risk of transmission of HIV to the foetus.
10

II. EPIDEMIOLOGICAL APPROACH TO THE HIV-AIDS THEORY

HIV is attached to AIDS to indicate that HIV is the cause of AIDS, and that is because
there was a time when there was only AIDS, and the cause of the syndrome was thought
to be something other than HIV.
An accidental transitory disease that attacks large numbers of people at the same time
and in the same country, region or place, is called an epidemic. Epidemiology is the
science that deals with epidemics.
Medical science has long known about epidemics and has developed a very precise body
of principles and rules by which it is possible, when applied to the phenomenon under
scrutiny, to deduce by their distribution patterns the nature of the cause of a particular
pathology which occurs at the same time among large groups of people.
Let us therefore start by approaching the phenomenon of HIV-AIDS from an
epidemiological perspective.
That is to say, phenomenologicaly speaking, that we are going to look at its geographical
features:—where it happens, when it happens, to whom it happens, how it happens—
meaning, in Heideggerian terms, that we are looking for what is the “thereness” of the
phenomenon. Let us see, then, what the phenomenon tells us from itself, as it stands
alone as itself.

The geography of AIDS

It was the U.S. Centres for Disease Control (CDC) which first reported in 1981 the
growing number of male homosexuals, intravenous drug-users and some risk groups
such as haemophiliacs and recipients of blood transfusion who were affected by
previously known diseases such as: Kaposi’s sarcoma, bacterial and fungal
(pneumocystis and candida) pneumonia, oral yeast infections, diarrhoea, herpes,
tuberculosis, weight loss, toxoplasmosis, and so on.
What was new was that the diseases were accompanied by a particular depletion of a
group of immune cells—T4 lymphocytes—and that the epidemic spread non-randomly,
selectively targeting a very specific group of people. Assuming, because of the T4-cell
depletion, that immune deficiency was the common denominator, the Centres for Disease
Control named it Acquired Immune Deficiency Syndrome, or AIDS (CDC 1981 1b).
11
A similar non-random epidemic was also reported in Europe by the WHO, affecting
selectively the same group of people.
Then, in 1983, the French research group led by Luc Montagnier(5) and in 1984 the USA
group led by Robert Gallo(6) presented papers published in Science claiming that both
had isolated HIV.
The public announcement that HIV was the cause of AIDS was made in April 1984 at an
international press conference in Washington by the Secretary of Health and Human
Services, Margaret Heckler, and Robert Gallo, researcher at the National Institute of
Health.
They announced that a new type of virus—a retrovirus—was the agent responsible for
the epidemic.
As epidemiological features, viral and microbial epidemics have in common:
1) They rise exponentially and decline within weeks or months of infection. The classical
epidemic curve is a bell-shaped curve that expresses the rise reflecting the exponential
spread of the contagion, and the fall reflecting the resulting natural immunity of
survivors.
2) The epidemics spread randomly in the population.
3) The resulting infectious diseases are highly specific, reflecting the limited genetic
information of the causative microbe. As a consequence the viral diseases are typically
more specific than those caused by the more complex bacteria or fungi.
4) The microbial and particularly the viral epidemics are self-limiting and thus typically
seasonal, because they induce anti-microbial and viral immunity and also encounter
genetically resistant hosts.
Being an infective agent, when we refer the HIV viral hypothesis to the epidemiological
principles of infectious diseases, a particular contradiction begins to emerge. This is
because it goes against two of the most fundamental epidemic principles of infectious
diseases: firstly the HIV-AIDS epidemic is non-random, and secondly the development
of HIV-antibodies by the host, after the encounter with the virus, gives no natural
immunity.
12

Non-randomness

The first striking feature is the non-randomness of the epidemic. The sine qua non
condition for an epidemic to have an infectious agent as a cause, is that it is random.
More astonishing is that from its beginning to this day (24 years), the AIDS epidemics of
the USA and Europe have still remained highly non-random:
• “Approximately 90% of all patients in the USA and 90% in Europe
are males.
• About 2/3 of all AIDS cases are male homosexuals (82% of all
males).
• About 1/3 are male and female intravenous drug-users, 75% of which
are male.
• One per cent are haemophiliacs and other transfusion recipients.
• One per cent are children born to drug-addicted mothers.”
(World Health Organisation 2001 1a).
This also means that all of the heterosexual male cases are intravenous drug-users,
except for a small fraction of haemophiliacs. And all of the women are intravenous drugusers.
According to the WHO (report 2001, 1b), since 1981 the AIDS epidemics of the USA
and Europe increased steadily for a decade and, after reaching peaks in the early 1990s,
all declined to currently about 1/2 of their peak levels. By 2001 the U.S. epidemic had
generated a cumulative total of 816,149 AIDS cases, and the European epidemic
251,021 AIDS cases.
Not only the selective group distribution of the disease is non-random, but even the
disease is distributed non-randomly among the selected risk groups:
• “Kaposi’s sarcoma is exclusively diagnosed among the male homosexual risk
group regularly using nitrite inhalants. The rest of the most common diseases in
the homosexual group are lymphoma, dementia, weight loss, yeast infections and
pneumocystic pneumonia.
• The children from mothers using psychoactive drugs during pregnancy commonly
present: bacterial pneumonia.
13
• Among the intravenous drug-users and ‘crack’ (cocaine) smokers, tuberculosis,
pneumocystis pneumonia and dementia are more prevalent than in any other risk
group.
• Haemophiliacs and other transfusion recipients in the USA and Europe usually
develop: pneumonia and yeast infections.
• The non-random distribution of these diseases in different risk groups, then and
now, suggests risk-group-specific causes, rather than a common one.”(106)
Another reason why the non-random feature of the epidemic is extremely interesting is
because it implies that if the cause of the epidemic is the HIV virus, the virus, quite
extraordinarily, is able to discriminate among its victims:
Discrimination by life-style (behaviour patterns): It has a particular tropism for a specific
and limited group of people, as we have just mentioned (homosexuals, intravenous drugusers,
haemophiliacs, and so on).
Discrimination by gender: 90% men (82% of whom are homosexuals), 10% women
(almost all of whom are intravenous drug-users).

No natural immunity

All viruses are most pathogenic prior to anti-viral immunity—before the body’s immune
cells have identified them. Once the viral proteins have been spotted, the defence
mechanism responds by producing a very specific group of antibodies, IgG, against these
viral proteins, and the virus is neutralised. The whole rationale of immunisation is
precisely to give the immune system the possibility to pre-empt the attack of a virus by
creating in advance antibodies against the virus. So the antibodies are the confirmation
that the patient has developed immunity to the virus.
By definition, HIV-AIDS is observed only after HIV immunity is established, that is,
after the development of those antibodies which later are detected by a positive HIV test
result. Ironically, in this case, antibodies do not mean immunity at all, but in fact quite the
opposite: they are the confirmation, by definition, of a fatal disease.
Yet at the same time it is very difficult to find the virus in AIDS patients.
“HIV can only be ‘isolated’ from rare, latently infected lymphocytes that are
cultured for weeks in vitro, away from the antibodies of the human host.”(107)
14
Even in patients dying from AIDS, less than 1 in 500 of the T4 lymphocytes that become
depleted are ever infected by HIV.(108) Currently, this difficulty in finding the virus would
be a confirmation of natural immunity, meaning that the antibodies are so effective that
no HIV is detectable in the AIDS patient. Yet, in spite of the presence of the antibodies
against HIV-proteins, the immune system continues to show low counts of T4
lymphocytes. If the decrease of T4-cells is due to the action of HIV, natural immunity in
this case, for some reason, is no longer efficient.
Unless we now begin to revise the foundations of immune response, we may have to
admit that either a) these antibodies are not against viral proteins and for that reason
cannot kill the virus, or b) that there is no virus to be killed, meaning that the proteins
which the antibodies are against, are not from HIV, and that is why HIV is so difficult to
find.
Since 1984 researchers have been trying, still with no success, to develop an AIDS
vaccine.
One might imagine that since the HIV virus has such peculiar characteristics, developing
a vaccine would never be possible, because in the case of HIV natural immunity is
inoperative.
These extremely specific features of the AIDS epidemics in the USA and Europe would
suggest that it cannot be produced by an infective, transmissible agent.
Having said all that, the puzzling epidemiological picture becomes even more peculiar
when we look at the epidemic in Africa.
The African epidemic, it is claimed, emerged in sub-Saharan Africa from 1984 onwards,
and according to the WHO increased until the early 1990s, similar to the epidemics of
the USA and Europe, but has since levelled off to cause about 75,000 deaths annually
(WHO 2001 1b). By 2001, Africa had reportedly seen a cumulative total of 1,093,522
cases (deaths) (WHO 2001 1b).
The African epidemic contrasts in its features very sharply with its American and
European counterparts:
• The first striking picture is that the African HIV virus no longer discriminates by
gender, precisely one of the more peculiar characteristic of U.S./European HIV.
In the sub-Saharan region of Africa, the AIDS epidemic is randomly distributed
between sexes.
15
• The second striking feature to reveal an enormous difference between the
U.S./Europe epidemic and the African one is that in Africa, the AIDS epidemic is
not restricted to behavioural risk groups, whereas in the U.S./European case, the
epidemic is almost entirely limited to a very specific risk group.
• The third difference of the African epidemic involves the diseases that the African
AIDS produces. The African epidemic is a collection of long-established
indigenous diseases, such as chronic fevers, weight loss syndrome (slim disease),
chronic diarrhoea and tuberculosis. The predominant and most distinctive AIDS
diseases in the U.S./Europe epidemic, pneumocystis carinii pneumonia and
Kaposi’s sarcoma, are almost never diagnosed in Africa.(106)
Reflection on this paradoxical epidemiological evidence suggests that the paradox may
not be created by the evidence itself, but rather by the correlation made of this evidence
under one single definition, that is, the affirmation that these diverse phenomena are
caused by one single transmissible agent: the HIV retrovirus.
Indeed, there are no paradoxes in nature: only flawed hypotheses.
Having assessed that it may be the definition that creates the apparent paradox, we need
to look now at the evidence that sustains that definition: the theory of HIV-AIDS, and
more particularly its most defining tool of all, the HIV test, to see if the phenomenon can
reveal itself, from itself, as itself.
16

III. MORPHOGENESIS OF THE HIV-AIDS THEORY

Cancer research

In modern medical text books we find, under the grouping of RNA viruses, the
retroviruses. More specifically, the ‘human lymphotropic retroviruses’, whose name
indicates their affinity to lymphocytes:
• HTLV-I and II are oncoviruses and are described as lymphocytic, meaning they
stimulate the production of lymphocytes, causing a malignancy of the T CD4
lymphocytes called human T-cell leukaemia-lymphoma.
• HIV-1 and HIV-2 are lentiviruses (slow viruses) and are lymphopenic, meaning
they destroy lymphocytes, causing AIDS.
All of these were discovered by the same man: Robert C. Gallo.
Robert Gallo was a man in pursuit of a particular type of virus: a retrovirus with
cancerous capacity. Robert Gallo, researcher at the National Institute of Health, was one
of the many virologists involved in President Nixon’s decade of War Against Cancer.
In the mid 1970s Gallo claimed to have discovered the first human retrovirus in patients
with leukaemia. He called the retrovirus HL23V.(1, 2)
Years later, when AIDS started to emerge, the first patients reported to have developed
AIDS in the USA were young male homosexuals suffering from pneumocystic
pneumonia and/or Kaposi’s sarcoma, a rare form of cancer otherwise only observed in
elderly people. The young age of the patients, alongside the disease’s particular tendency
to affect the lungs, made these cases even rarer. To oncovirus researchers like R. Gallo,
these appeared potentially to be the work of a retrovirus.
Theory means ‘to look at’. From where you look, you see. The platform from which this
phenomenon was observed, was cancer research.
Retroviruses are the offspring of cancer research.
The hypothesis that infectious agents could produce cancer had been on the scientific
horizon for quite some time. Research on animal tumour-cells by Ellerman and Bang in
1908, and by Rous in 1911, led to the first description of an agent separable from the
tumour cells that could induce, following inoculation, leukaemia or sarcoma in healthy
animals. In neither case did the malignancies occur naturally, rather the experiments
17
entailed the production of acellular ultra-filtrates from artificially leukaemia-inbred
laboratory chickens or induced sarcomas on a laboratory fowl. Since the ultra-filtrates
contained no cells, the information had to come from genetic material, and the hypothesis
was that the agent had to be a virus.
In the 1950s Ludwick Gross found retroviruses that caused tumours in mice and chicken.
All the animals in the retrovirus studies were inbred laboratory strains. Moreover, many
of the infections were congenital.
From 1955 onwards, under the direction of James Shannon, the USA’s National Institute
of Health (NIH) promoted cancer research and received extraordinary budgets from
Congress to finance major programmes in the fight against cancer. These included the
search for oncoviruses and the development of cancer drugs.
In 1960 the feline leukaemia virus (FeLV) was discovered by W. Jarret. The virus was
capable of causing not only malignancies in blood cells, but also aplasias (insufficient
growth of affected cells) and an immune deficiency.
All of these animal oncoviruses are now classified as retroviruses.
All of the retroviruses had been found in lymphocytes. They were the outcome of
laboratory experimentation on animal lymphocytes, diseased by induction or naturally.
New hypotheses were developed in the 1960s by Duesberg that a virus could carry a
cancer gene (oncogene), and its introduction into the cell DNA would later be
responsible for that cell becoming cancerous. Peter Duesberg, a brilliant scientist from
Berkeley, had mapped a particular mutation to a single nucleotide in what was to become
known eventually as an oncogene. Duesberg was named California Scientist of the Year
for developing the theory that oncogenes might be introduced by viruses into humans
and cause cancer. Years later Duesberg found flaws in his own theory and announced
this to his surprised colleagues, who were working on demonstrating that it was highly
unlikely. Despite this, research on the viral oncogene hypothesis continued fruitlessly for
the next ten years.
It is important to point out at this stage that these viruses were thought to be exogenous
viruses, meaning they come from the outside. However, the human organism also
contains internal, or endogenous, viruses. Our bodies contain countless retroviruses,
which have been in the human genome since the beginning of human life. Endogenous
retroviruses are regarded as evolutionary genetic remnants, bits of DNA or RNA seen as
viruses, whose genetic material is attached to the main DNA of the cell and has been
found in the chromosomes of many animal species. They are transmitted to other
18
members of the species through ordinary Mendelian inheritance, or directly from the
mother in the form of new viruses—infectious viral particles that can pass from mother
to foetus. In 1969, Robert J. Huebner and George J. Todaro of the National Cancer
Institute proposed that the activation, by carcinogens, of these normally silent
endogenous sequences was the mechanism of all malignancies.

Retroviruses

A virus is not a cell but a microscopic particle with a coat made of a few proteins (a
given species of virus is always of the same form and size), strung around a piece of
RNA or DNA that contains genetic information (for a given species of virus, this is
always of the same length).
Retroviruses are viruses that have RNA as a genetic material.
Retroviruses are incredibly small—about 100 nanometres in diameter—and can only be
seen through an electron microscope. They are almost spherical, and have an outer
envelope covered with knobs and an inner core consisting of some proteins and RNA.(9)
Retroviruses are classified into three Subfamilies:
• Spumavirinae
• Lentivirinae (HIV I, HIV II)
• Oncovirinae—type A, B, C and D particles
In the 1970s such particles were frequently observed in human leukaemia tissues,
cultures of embryonic tissues,(53, 54) and in the majority of, if not all, human placentas.(55)
These findings led to a very interesting view among certain retrovirologists, which was
this: because retroviral genomes may arise from the rearrangement of cellular DNA
caused by numerous factors, including pathogenic processes, retroviruses may be more
of an effect than a cause of disease.(56, 57) “The human genome carries DNA sequences
related to endogenous retroviral genomes that are subdivided into families according to
sequence homology. Some are present in only a few copies, whereas others are present
in hundreds to thousands of copies.”(58)
19
Viruses are stable, because they have to leave cells or even the organism to infect other
cells or organisms anew. Unlike cells, viruses do not have any of the cellular structures
(mitochondria, ribosoma, etc.) that allow a cell to survive and reproduce. Therefore, in
order to reproduce themselves and express the genetic information that they carry, they
need to parasitise cells.
The protective coat of the viral particle fuses with the cell membrane, then the particle
passes inside. Once inside, its genetic information gets into the cell nucleus, becomes part
of the cellular DNA, and takes over the cell’s metabolic machinery for its own benefit, by
which process the virus particle is disassembled. Then, using the same machinery,
separate pieces of new virus are synthesised. Later, all the viral components are put
together and the new virus particles are ready to free themselves, either by destroying the
host cell or, in the case of retroviruses, by a more conservative process of budding out of
the cell membrane. This particular characteristic of needing to parasitise cells makes
viruses a difficult target for specific therapeutic agents. Anti-bacterial drugs like
antibiotics attack their bacterial targets with tremendous specificity (until, of course, the
bacteria develop antibiotic resistance!) Nevertheless, by killing specifically bacteria, they
do not cause too much damage to the host’s body. In the case of viruses, an anti-viral
drug would need to discriminate between the proteins and DNA made for viruses, and
those proteins and DNA made for their human hosts.

The discovery of reverse transcriptase (RT)

For most of the cells in all living things, the direction of information flow is from the
DNA of the nucleus to the RNA in the cytoplasm. In the nucleus the DNA duplicates
itself, then this copy, after being trimmed by an enzyme, is released into the cytoplasm
and becomes RNA, by which the genetic message is transported from the nucleus to a
cytoplasmic structure called ribosome, where the protein synthesis will take place
according to the instructions that the RNA carries.
Retroviruses have their name because, unlike other viruses, the transfer of information is
‘backwards’.
In the 1970s there were many scientists engaged in the ‘War Against Cancer’. This
experimental work led to two crucial discoveries: the finding of reverse transcriptase in
1970, and of interleukins in 1976.
In 1970 the enzyme reverse transcriptase (RT) was discovered in oncoviruses, which
from then on became known as retroviruses. Howard Temin was awarded the 1975
20
Nobel Prize for Medicine for that discovery. The popularity of this unique retroviral
enzyme (as it was then assumed to be), caused many virus researchers to switch to the
retroviral quest. One of the major reasons for the interest was that this fundamental
enzyme could be a specific target for the drugs against the virus. So, while there were
people looking for diseases that might be caused by retroviruses, alongside, the
pharmaceutical industry was already developing anti-retroviral drugs, drugs that could
interfere with reverse transcriptase. The famous AZT, the first drug claiming to treat
AIDS, was produced in 1964.
Retroviruses do not carry DNA as a genetic material, rather RNA.
Retroviruses do not use their RNA blueprint directly to make more viruses. Once they
enter a cell, retroviruses first make a DNA copy of their RNA. This process, called
reverse transcription, is catalysed by the enzyme called reverse transcriptase (RT). This
DNA then moves into the cell nucleus where it becomes part of the cellular DNA. This
string of DNA is called a provirus, and sits there, hibernating as it were, for a long time,
perhaps several years, until something activates the cell. Then the pro-viral DNA is
copied back into RNA and it is this RNA, not the original RNA that entered into the cell
when it was parasitised by the virus, which instructs the production of the necessary
proteins to make new viral particles.
So the detection of reverse transcriptase became the blueprint for the confirmation of the
existence of a retrovirus. “Since reverse transcriptase is unique to retroviruses, finding it
in tumour cells would show that such a virus was there.” (R Gallo, 1986, ‘The first
human retrovirus’, Scientific American, p. 91). In the same article the author mentions
that from leukaemia cells of a few patients, they purified DNA polymerases that seemed
to have all the properties of reverse transcriptase. He then goes on to say, “The enzymes
might have been unusual cellular polymerases detectable only because their numbers are
increased in diseased cells,” meaning natural enzymes from the main tumour cells.
Ever since then, the standard technique for detecting retroviruses has been the analysis of
the activity of reverse transcriptase in cell cultures.
Unfortunately, in the 1970s, the biochemical function of reverse transcription did not fit
the dominant world picture of genetics and was thought to be exclusive to the new class
of viruses, the retroviruses, which is why the detection of reverse transcription was
henceforth accepted as a ‘proof’ of the presence of a retrovirus. But in 1990s it was
established that the biochemical process of reverse transcription is a natural cellular
function that reflects a repair mechanism for damage to cellular genetic material.(102)

The discovery of interleukins

21
The discovery of reverse transcriptase as the supposed indicator of the presence of a
retrovirus heightened the search for human retroviruses, and led to the development of
molecular biology techniques aimed at detecting low-levels of reverse transcriptase
activity.
The hypothesis on human retroviruses was that they were slow viruses that required a
long time to emerge, and it was therefore thought necessary to keep the cells alive for
long periods of time in order to detect low levels of virus expression. Human blood cells,
normal or cancerous, are difficult to grow in the laboratory. Prior to 1976 it was
impossible to grow lymphocytes for long enough. The discovery of growth factor
proteins was the answer. Gallo and his colleagues found that after the stimulation of
T lymphocytes with a protein called phytohemaglutinin (PHA) derived from plants, Tcells
would release a growth factor, now called interleukins 2 (IL-2), that would induce
T-cells to divide and mature.
This was a crucial step. The discovery of IL-2 could be used to grow T-cells in the
laboratory long enough to see if any retroviral presence would emerge.

Standard identification of a retrovirus

Three steps must be fulfilled in order to prove the existence of a retrovirus:
1. Culture cells and find a particle that looks like a virus. Physical-electron
microscopy for virus count, morphology and purity.
2. Use the standard method to isolate the particle, break it into pieces, and
analyse its make-up. Biochemical reverse transcriptase activity, viral and
cellular RNA, total protein, gel analyses of viral and host proteins and nucleic
acids.
3. Prove that the particle in question can make faithful copies of itself, in what
is known as ‘replication’. Biological infectivity in vivo and in vitro.
Explanation:
Identifying a retrovirus requires an electron microscope and a high speed centrifuge.
Retroviral particles have a physical property—their buoyancy—which enables them to be
separated from other material in cell cultures. This is utilised to purify the particles by a
process called ‘density gradient centrifugation’.
22
The identification process begins by growing cells that are believed to contain
retroviruses. The retroviral particles will then be released from the cells into the culture
fluids. After decanting a specimen of culture fluids, a drop is placed on top of a solution
of sucrose in a test tube. This is a solution that is light at the top but gradually becomes
more dense towards the bottom. Then the test tube is spun at extremely high speeds.
This generates tremendous forces, and particles present in the drop of fluid are forced
through the sugar solution until they reach a point where their buoyancy prevents them
from penetrating any further, meaning a place at which their own density is the same as
that of the sugar solution. They ‘band’ at a point where the density is 1.16 g/ml. That
band can then be selectively extracted and photographed with an electron microscope.
This band, however, is not specific to retroviruses alone, but only to a particular
molecular weight.
The next step is to disrupt the particles, find out what proteins and RNA they contain,
and prove that one of the proteins is reverse transcriptase that turns RNA into DNA.
Finally, PURE particles have to be added to a culture of un-infected cells to see if they
can replicate themselves and produce the same particles with the same constituents.
Replication is paramount in order to be 100% certain that a retrovirus has been
identified, because retrovirus-like particles are not the only material that may find its way
into this band of the density gradient. Very small cellular particles, some recognisable as
internal cellular structures, or just cellular debris, can also band at 1.16 gm/ml, and some
of this material can even enclose nucleic acids (DNA and RNA) and take on the
appearance of retroviral particles.
23

IV. ANALYSIS OF THE EVIDENCE OF THE HIV-AIDS PHENOMENON

A modern clinical medicine textbook, under the heading ‘Diagnosis of HIV infection’,
indicates:
“HIV infection is diagnosed either by detection of virus-specific antibodies
(anti-HIV) or by direct identification of viral material:
- Detection of IgG Antibody to gp120 and its subunits. This is the most
common marker of infection. The routine tests used for screening are based
on ELISA techniques that may be confirmed with Western Blot assays. Up
to 3 months may elapse from initial infection to antibody detection
(serological latency). These antibodies to HIV have no protective function
and persist for life. As with all the IgG antibodies, the anti-HIV antibody will
cross the placenta. All the babies born to HIV infected women will thus have
the antibody at birth. In this situation, the anti-HIV antibody is not a reliable
marker of active infection [i.e. the development of AIDS diseases] and in uninfected
babies will be gradually lost over the first 18 months of life.
- Detection of IgG antibody to p24. The anti-p24 antibody can be detected
from the earliest weeks of infection and through the asymptomatic phase. It
is frequently lost as disease progresses.
- Antigen assays are nucleic acid-based assays that amplify and test for
components (PCR, viral load) of the HIV genome. All are based on HIV-1
subtype B material, and there are potential inaccuracies with other subtypes,
especially group O variants. These assays are used to aid diagnosis of HIV in
the babies of HIV-infected mothers, or in situations where serological tests
may be inadequate.
- Viral p24 antigen (p24ag). This is detectable shortly after infection but
usually disappears by 8-10 weeks after exposure. It can be a useful marker in
individuals that have been infected recently but have not had time to mount
an antibody response. It may reappear at low levels intermittently during the
period of clinical latency, and in some people as infection progresses.
- Isolation of virus in culture. This is a specialised technique available in
some laboratories to aid diagnosis and as a research tool.”(131)
24

A) HIV IDENTIFICATION

As we have mentioned before, the three known human retroviruses were reported by the
same man: Robert C. Gallo. They are HTLV-I and II, and HTLV-III or HIV-1.
HTLV-I and II are oncoviruses and described as causing lymphocytosis, meaning they
stimulate excessive production of lymphocytes.
HTLV-III, better known as HIV, is a lentivirus (slow virus) and is lympholytic, meaning
it destroys lymphocytes. Since a second strain of HIV has been reported, mostly in west
Africa, HIV is now being described as HIV-1 and HIV-2.
R. Gallo is important because, historically, he was a man looking at the phenomenon
from a particular perspective, and he was fundamental in the development of the arena in
which that perspective unfolds, which is the laboratory technique of the continuous
growth of leukaemia T-cells in the artificial medium of a test tube.
The experiment and the experimenter are part of the same reality. In this sense one could
say that R. Gallo developed his own method of identifying the virus.
In the mid-1970s Gallo claimed to have discovered the first human retrovirus in patients
with acute myelogenous leukaemia. He called the retrovirus HL23V.(1, 2)
Gallo used nothing more than antibody reactions to ‘prove’ which of the proteins
(antigens) in the cultures were viral proteins. This is an indirect way of identifying a
virus. The presence of the antigen revealed by the antibody does not prove the origin of
the antigen itself, therefore it may not be specific to retroviruses. Because it avoids the
proper standard scientific method of isolation and identification of the retroviruses, the
evidence is not conclusive.(7,8)
Not long afterwards, other researchers claimed to have found the same antibodies in
many people who did not have leukaemia. A few years later these same antibodies were
shown to occur naturally and to be directed against many substances that had nothing to
do with retroviruses.(3, 4) It was realised that HL23V was a mistake.
In 1980, Gallo and his group presented the discovery of another retrovirus, and this time
he called it HTLV-I.(2b) The procedure utilised for this ‘isolation’ was the same one as
before. He claimed that it caused a particular rare form of leukaemia that was then
named ‘adult T4-cell leukaemia’ or ATL, in which T4-cells are present in excessive
amounts. Apart from being medically irrelevant, the HTLV-I discovery was again
nothing more than experimental data from leukaemia patients, as was his former HL23V.
The greatest prevalence of HTLV-I was reported in Africa and Southern Japan, and that
25
is where it remains prevalent. Yet although this virus is said to cause leukaemia, less then
1% of persons who test positive to the test ever develop leukaemia. In 1982 a new
subtype of human T-cell leukaemia virus (HTLV-II) associated with a T-cell variant of
hairy cell leukaemia was discovered by Gallo and collaborators.(2c)
The reason why retrovirologists became interested in AIDS was that Kaposi’s sarcoma
(KS), a rare form of cancer only observed in elderly people, was one of the first of the
most common shared diseases among those young male homosexuals suffering from
AIDS in the United States. The young age of the patients, as well as the new peculiarity
that KS was affecting the lungs in all of these cases, made it even more exceptional. So
to oncovirus researchers, these cases, sharing as they did the same rare type of cancer,
and all being promiscuous young male homosexuals, indicated that the cancer might be
transmitted—sexual transmission perhaps—therefore an infectious agent. And that
would fit the retroviral hypothesis.
The actual identification of the retrovirus HIV, surprising though it may be, does not
follow the standard method of retroviral isolation explained earlier, but instead by-passes
major steps, casting doubt on the evidence itself.
It is important to go back to the experiments that were done in 1983-84, because
everything believed and taught about HIV is founded on what happened then.
In 1983 Luc Montagnier from the Institute Pasteur in Paris presented a paper(5) claiming
that he had isolated a retrovirus from a lymph node of a homosexual decorator with
AIDS. He called it the ‘lymphadenopathy associated virus’ (LAV). Note: to this French
researcher, the virus was not yet a causative agent but an associated one. The causative
agent view only emerged some time later, when Gallo patented the HIV-test made with
proteins that allegedly came from Montagnier’s sample. Montagnier had sent
supernatants from LAV-1 ‘infected’ cultures to Robert Gallo at the National Institute of
Health in the USA for evaluation. Later on Montagnier was to sue Gallo for
misappropriating his strain.
Gallo’s isolation was almost a carbon copy of his first two failed attempts to isolate a
retrovirus in his war against cancer, HL23V, and HTLV-I and its later variety HTLV-II.
In fact, some of these early efforts were scientifically more soundly conducted than the
infamous HIV procedures.
The identification of the HIV virus stands on three main evidences:
1: Electron micrographs of retroviral particles
2: Finding reverse transcriptase
26
3: Antibody reaction to HIV proteins

1: Electron micrographs (EMs)

In 1973 the Pasteur Institute hosted a meeting attended by a number of scientists, some
of whom are now among the leading HIV experts. At that meeting the method of
retroviral isolation was thoroughly discussed, and the photographing of the 1.16 band of
the density gradient was considered absolutely essential.
Surprising though it may seem, Luc Montagnier and Robert Gallo published electron
micrographs (EMs) of a few particles in cultured fluid that they claimed to be the HIV
retrovirus,(5, 6) and everyone subsequently called it ‘pure HIV’. However, they did not
publish any EMs of the material at the 1.16 gm/ml band density gradient as the retroviral
scientific method requires, let alone prove what the particles were.(10) Even more
puzzling is that, up until March 1997, all of the electron microscope pictures published
were from un-purified cell cultures, not from the density gradient.
Animal retrovirologists are well aware of the importance of obtaining retroviral particles
without disrupting the cells in order to avoid cellular contamination, which is why they
strongly advise handling the cultures gently and regularly topping them up with nutrients
to keep the cells alive so that they do not disintegrate. But in most of the HIV
experiments the cells are deliberately broken up by the experimenter as part of the
experiment.
Moreover, if HIV is cytopathic as it is believed to be, it means that it destroys cells,
Lymphocyte T4-cells, and it would be very difficult to claim that the putative virus
particles are the only things likely to be floating around in cultured fluids or at the 1.16
gm/ml density gradient.
Finally, in 1997, two groups, a Franco-German one(12) and one from the U.S. National
Cancer Institute(13) published pictures of the density gradient band. The Franco-German
study pointed out that cell membrane vesicles are a major contaminant of the gradientenriched
human immune deficiency virus type-1 (HIV-1) preparations, and their pictures
revealed that the vast majority of the material in the density gradient is cellular, therefore
non-viral. The American study, in which it is impossible to tell from which density
gradient the pictures are taken, concede that those micro vesicles (encapsulated cell
fragments) are a source of contamination of cellular proteins found in purified HIV-1
preparations. So both say that their samples might be contaminated.
27
Yet the researches claim that the few particles that appear in the pictures are retroviral
HIV particles. They do not give any evidence why. Also, it would be expected that if the
sample were to contain retroviruses, billions of particles would be found, not just a
few—yet that is not explained either. Although these few particles may look like
retroviral particles, they may also not be. The only definitive proof that they are
retroviruses would be if they were capable of self-replication, which again was not done
in any of the studies.
Regarding the morphology of retroviruses, most retrovirologists agree that retrovirus
particles are almost spherical in shape, have a diameter of 100-120 nanometres, and are
covered with knobs.(9, 11) But in these two studies the particles that are claimed to be
retrovirus are not spherical, the diameters exceed twice that permitted for retroviruses,
and none appear to have knobs.
The Franco-German particles are 1.14 times larger than the known retroviral particles
and therefore have 50% more volume than a normal retrovirus and the American
particles are 1.96 times larger, meaning they have 750% more volume, so the American
particles are five times more voluminous than the Franco-German ones.(109) This is
particularly crucial: because density is the ratio of mass to volume, if the volume is up, to
keep the same density, the mass has to go up by the same amount. Any genuine retroviral
particle will contain a fixed amount (mass) of RNA and protein—no more, no less—yet
the particles presented in these two studies are made up of much more material. This
means that if these different sized particles are truly HIV, then HIV cannot be a
retrovirus, and the specific 1.16 gm/ml density band which is characteristic of
retroviruses and which is employed to determine HIV, can no longer be used, unless we
begin to redefine retroviruses and their means of identification. This is the band on which
all the major research on HIV has been done for the last 15 years, and, moreover, it is
the band used to obtain proteins and RNA as diagnostic agents in the HIV-test to prove
HIV infection.
The other possibility, of course, is that the electron micrographs of that study are not
from the 1.16 gm/ml band, in which case the particles are obviously not retroviruses.
Another problem arises related to the absence of knobs in the particles of these two
studies. All of the AIDS experts agree that the knobs are absolutely essential for the HIV
particle to lock on to a T-cell. The knobs of retroviruses contain a protein called gp120,
which is the hook in the knobs that grabs hold of the surface of the cell that it is about to
infect.(14) So, if the HIV particles do not have knobs, it is very difficult to explain how
they can attach themselves to a cell and parasitise it.
28
On the evidence provided by these pictures it is impossible to explain the claim that this
material is pure, or that it contains even retrovirus-like particles, let alone the specific
retrovirus HIV.

2: Finding reverse transcriptase (RT)

The current way to prove the presence of RT is indirect. Reverse transcriptase is not
isolated as such, but if a template of RNA is introduced into a solution suspected of
containing RT, the enzyme will reveal its activity and therefore its presence by
transcribing the RNA into DNA.
It is of the greatest importance, when trying to detect the activity of reverse
transcriptase, that the natural genetic messenger material is used—the RNA-genome of
the virus that should be there if the virus exists. Despite this, all HIV researchers always
use, without any explanation as to why, synthetic messenger material templates. This is
so crucial because those templates are not specific to reverse transcriptase alone: on the
contrary, they are efficiently recognised and transcribed by normal, common, cellular
genetic material-producing enzymes such as DNA-polymerases.
Gallo’s group began culturing lymphocytes from AIDS patients, but none of the cultures
produced enough reverse transcriptase to prove that a retrovirus was present. Then
Gallo and another researcher from his group, Mikulas Popovic,(6) made a preparation
consisting of a mixture of culture fluids from ten AIDS patients and added that to a
culture of leukaemia cells, HUT78 cell, which had been obtained years earlier from a
patient with malignancies of mature T4-cells, called adult T-cell leukaemia (ATL).
However, these leukaemic cells were supposed to already contain the retrovirus HTLV-1
of which Gallo had presented the genetic sequences in a paper published a year earlier
(1983) in Nature.(15) This time enough reverse transcriptase was produced for them to
believe they had a retrovirus. It is difficult to know if the reverse transcriptase was from
the presence of HIV, or HTLV-1, or neither of them.
Popovic also made a clone of the same leukaemia cell line, the HUT78 cell line, called
the H9 clone. Evidence exists that the H9 cell line releases retrovirus-like particles even
when not ‘infected with HIV’.(103) The H9 clone has since then been widely used, both in
research and commercially for producing what are regarded as the HIV proteins for use
in the antibody test kits. Interestingly enough, although HIV is thought to kill T4-cells,
the leukaemic cell line as well as its H9 clone are both immortal even when infected with
HIV. So these cells permit what is believed to be HIV to grow indefinitely. The proteins
29
produced from these cells are the ones patented by R. Gallo as the antigens for testing
antibody reaction to HIV. All of the test kits for HIV come from these proteins.(110, 111)
As mentioned above, the existence of reverse transcriptase is proven indirectly by
introducing a synthetic piece of RNA (An.dT15) into a culture and seeing if DNA
bearing the corresponding sequence appears. In all HIV research, the copying of the
template-primer An.dT15, when incubated with supernatant or the material that bands at
1.16 gm/ml from AIDS cultures/co-cultures, is considered proof of HIV reverse
transcriptase activity. So it is measured by demonstrating the process of reverse
transcription, which is what the enzyme does, but not by measuring the actual enzyme
itself. That is why the same template is also copied when incubated with material that
bands at 1.16 gm/ml from leukaemia T-cell cultures,(49) and normal non-infected
spermatozoa.(50) Both An.dT15 and Cn.dG15 are also copied by material that bands at
1.16 gm/ml (the retroviral band) originating from normal non-infected but mitogenically
stimulated lymphocytes.(49, 51) Furthermore, An.dT15 is copied not only by reverse
transcriptase but also by two (beta and gamma) of the three cellular DNA polymerases.
In fact, DNA polymerase is a cellular enzyme that copies An.dT15 with high efficiency
but which does not copy DNA well.(52) Thus, the copying of the template An.dT15
cannot be considered synonymous with the presence of HIV reverse transcriptase.
There is a problem emerging here, because the laboratory techniques that are supposed
to be direct and specific as the hallmark of retroviral-HIV identification, are not:
Firstly, reverse transcriptase is not unique to retroviruses. Reverse transcriptase is
present in normal cells and also in bacteria.
Secondly, reverse transcriptase is not the only substance capable of producing reverse
transcription. Normal cellular enzymes can also do it, as we have mentioned above. In
fact they do it very well with the very same synthetic RNA (An.dT15) that all HIV
researchers introduce into their cultures to copy into DNA.(16) It is known also that some
of the chemicals that are an obligatory component of these cell cultures cause normal
lymphocytes to reverse transcribe.
Even more important is the fact that leukaemia cells can also produce reverse
transcription unaided, when not cultured with such chemicals or cells from AIDS
patients.
In fact, reverse transcription is now known to reflect a repair mechanism for damage to
cellular genetic material in normal cells.(102) So it is perfectly obvious that finding reverse
transcriptase, less still by merely showing that reverse transcription is taking place, is not
enough to prove the presence of a retrovirus.
30
Retrovirus-like particles are found practically everywhere. In the 1970s such particles
were frequently observed in human leukaemia tissues, in cultures of embryonic tissues,
and in the majority of animal and human placentas. These findings are of extreme
significance because the H9 cell line (the clone cell line which is the source of all of the
proteins for the HIV test) is made up of leukaemia cells. They are also important because
Luc Montagnier obtained his EMs from cultures produced using umbilical cord blood
lymphocytes. In 1988, a study by researchers from Harvard(17) reported the finding of
retrovirus-like particles, or ‘HIV particles’ as they were called, in 90% of enlarged lymph
nodes from both AIDS and non-AIDS patients.

3: Antibody reaction to HIV proteins

The Gallo hypothesis is that there is a virus causing AIDS, and it is foreign, so when it
infects a person that person develops antibodies to the virus.
Using antibodies to prove the existence of a virus is the key part of the problem, since it
is an indirect method that in itself only proves that a reaction is taking place, but does not
confirm the origin of the protein that triggers that reaction.
Viral proteins are those proteins that come out of particles proven to be viruses. But in
order to define the proteins of a retroviral particle, first it has to be proven that the
particle in question is a retrovirus. What may not be done is to assume that the protein
comes from a retroviral particle, and to then use the antibody reaction to the protein as
proof of the identity of the particle if we do not yet know the identity of the protein in
the first place.
Antibodies are imprecise because they do not react only to single proteins.(18, 19) In what
immunologists call cross-reactions, an antibody reacting to a protein in a culture could
just as well be an antibody made to counter something totally unrelated. And if we are
trying to define which proteins are unique constituents of a retroviral particle, it cannot
be proven by performing chemical reactions on what is essentially a culture soup. In that
case antibodies are completely irrelevant.
What the experiments reported in the first Gallo paper really tell is that some antibodies
present in a patient with haemophilia, as well as in rabbits, reacted with some proteins in
H9 cells (a clone of leukaemia cells) cultured with lymphocytes from AIDS patients.(6)
These reactions do not say anything about the identity of the proteins coming from the
H9 cells (are they cell proteins or viral proteins?) nor about the specificity of the
antibodies from the haemophilic patient (are they against a cell protein or a viral
31
protein?) Antibodies can only be specific to HIV if, and only if, they are present ONLY
when HIV is present. This means that we need to have proteins that we are 100% certain
belong only to HIV.
It is therefore quite clear that it is impossible to prove the origin of a protein by an
antibody reaction, if you have not first identified the source of the protein.
What we have are some cultures of tissues derived from AIDS patients that react with
antibodies present in the serums of AIDS patients. We know that AIDS patients are
infected with many different agents. So if these agents, or bits of them, are present in
AIDS patients, they will also be present in their cell cultures. Everyone agrees that AIDS
patients have myriads of antibodies to all manner of things, including antibodies to
human T-cells, the cells that make up the cultures. If we add some antibodies from the
same kind of patients to these cultures, all we see are reactions: we cannot tell what is
reacting to what.
A good example of this is the hepatitis B virus (HBV). Many AIDS patients, and in the
case of haemophiliacs virtually all of them, are infected by HBV. And HBV does not just
infect liver cells, it also infects T-lymphocytes. Also, strange though it may seem, HBV
has a reverse transcriptase enzyme and people make antibodies against this virus.
The other puzzling aspect of the Gallo experiment(6) is that he claims he had serum from
rabbits that contained antibodies specific to HIV. They say that they had prepared rabbit
antibodies by repeatedly infecting rabbits with HIV.
Before he had a virus there was no way of knowing in advance that antibodies to HIV
existed at all. Anywhere. So if they were preparing antibodies to HIV they would have
had to inject rabbits with pure HIV, which means they would have had to have isolated
already that which they were in fact attempting to do for the FIRST time.
What Gallo and Popovic injected was their culture material, which at very best was a
banded 1.16 gm/ml specimen (a debris of proteins), something akin to what we see in the
Franco-German and U.S. National Cancer Institute pictures,(12, 13) which they and
everyone else have since regarded as pure HIV. Gallo and Popovic would have exposed
their rabbits to a multitude of cellular proteins. Proteins are the most potent antibodyproducing
substances available, even more if they are introduced directly into the bloodstream.
The rabbits would have then produced antibodies to all those proteins, and when
they added these antibodies back to the material they injected in the first place, there
would be reactions as you would have expected. That, however, does not make that
material injected into a virus.
32
And even to begin to talk about specific antibodies to specific HIV proteins, first it has to
be proven that the proteins are constituents of a retrovirus-like particle, and that that
particle is able to replicate. The virus is needed BEFORE looking for proteins and
antibodies, not the other way around.
Science is about evidence and proof. But for some unexplained reason the traditional,
logical, reliable, common-sense method of proving the existence of a virus has been
abandoned in the HIV era.

B) THE HIV-ANTIBODY TEST

The antibody test is the same procedure that was used to prove the existence of HIV in
cultures from AIDS patients by the French in 1983 and by the Americans in 1984. But it
is also the same procedure that Gallo and his colleagues used to prove the existence of
HL23V in the mid seventies,(1) which later proved to be a big mistake.
The problem with using antibodies is that there can be two types of antibodies. One type
is specific, meaning antibodies caused by HIV and nothing else, and reacting to HIV and
nothing else. The other type is non-specific, meaning antibodies caused by other agents
or stimuli, which certainly react to those agents, and also react to HIV.
The test is nothing more than a chemical reaction. Something changes colour. So when a
person’s serum is added to some of the so-called ‘HIV proteins’ in a culture or in a test
kit, and a reaction appears, it is impossible to tell which type of antibody is responsible
for the reaction. There are three possibilities: all the antibodies might be the specific type,
or none of them, or there might be a mixture. The only way to tell would be to test for
antibodies in all sorts of patients: some with AIDS, some who are ill but who do not
have AIDS, and some healthy people as well. And in all the experiments, at the same
time, HIV would have to be used as the adjudicator to determine what type of antibodies
they are. Only then could the test be introduced into medical practice as a diagnostic
tool. Yet that experiment has never been done.
Gallo only managed to isolate a retrovirus in 36% out of 72 AIDS patients, but 88% of
the patients had antibodies, which means that there were more patients with antibodies
but without viruses than there were patients with viruses. Yet Gallo filed a patent for the
antibody test the very same day that the idea of HIV as the cause of AIDS was launched
into the world, 23 April, 1984.
For the test, the patient’s blood is mixed with proteins acting as antigens extracted from
H9 or other cell cultures, and put all together in a test tube or separately at discrete
33
points along a thin paper strip. The first is called ELISA and the second Western Blot. If
the proteins react with the blood then the patient is reported HIV positive. The ELISA
test is used to screen for antibodies, and then ‘confirmed’ by the more specific and highly
sensitive Western Blot. The leaflet accompanying one such test kits says:
“The test for the existence of antibodies against the AIDS-associated virus is
not diagnostic for AIDS and AIDS-like diseases. Negative test results do not
exclude the possibility of contact or infection with the AIDS-associated
virus. Positive test results do not prove that someone has an AIDS or pre-
AIDS disease status nor that he will acquire it.”(20)

The antigens: the viral proteins

The proteins considered to represent HIV antigens are obtained from mitogenically
stimulated cultures in which tissues from AIDS patients are co-cultured with cells
derived from non-AIDS patients—usually established leukaemia cell lines. Following the
detection of the enzyme reverse transcriptase in the cultures (actually, not detecting the
enzyme itself, but the reverse transcription process with synthetic RNA), the cell lysates
are spun into density gradients. The material that bands at 1.16 gm/ml is considered to
represent ‘pure HIV’ and consequently the proteins found at that density are considered
to be HIV antigens. The immunogenic HIV proteins are thought to be coded by three
genes:(21)
Gag gene: codes for a precursor p53/p55, then cleaved to p24/p25 and
p17/p18.
Pol gene: codes for proteins p31/p32.
Env gene: codes the precursor protein p160, which is cleaved to p120
and p41/p45.
Montagnier’s group considered p24 sufficient to define a positive Western Blot (WB),
whereas Gallo’s group considered p41 sufficient. Most laboratories use the criteria
recommended by the Centres for Disease Control (CDC), namely the presence of a band
at either p24 or p41.
— The p41 protein
34
p41 is one of the proteins detected by both Gallo’s and Montagnier’s groups in the first
HIV isolates. However, Montagnier and his colleagues observed that AIDS sera reacted
with a p41 protein both in HIV and HTLV-I infected cells, as well as non-infected cells,
and concluded that the p41 band “may be due to contamination of the virus by cellular
actin which was present in immunoprecipitates of all the cell extracts.”(5)
Actin is a ubiquitous protein found in all cells as well as bacteria and several viruses. It is
also known that the oxidation of cellular sulphydryl groups, as in the case of AIDS
patients,(23) is correlated with the assembly of polymerised actin,(24) and that the level of
actin antibody binding to cells has been proposed as “a sensitive marker for activated
lymphocytes.”(25)
Platelets from healthy individuals also contain a p41/45 protein that reacts with sera from
homosexual men with AIDS and immune thrombocytopenic purpura (ITP) and which
“represents non-specific binding of IgG (antibodies of AIDS patients) to actin in the
platelet preparation.”(26)
— The p24/25 protein
Detection of p24 is currently believed to be synonymous with HIV isolation and
viraemia. However, apart from a joint publication with Montagnier in which they claim
that the HIV p24 is unique, Gallo and his colleagues have repeatedly stated that the p24s
of HTLV-I and HIV immunologically cross-react.(27)
Genesca et al(28) conducted Western Blot assays in 100 ELISA negative samples of
healthy blood donors. 20 were found to have HIV, with p24 being the predominant band
(70% of cases), leading them to conclude that “most such reactions represent falsepositive
results.”
Antibodies to p24 have been detected in 1 out of 150 healthy individuals, 13% of
randomly selected, otherwise healthy patients with generalised warts, 24% of patients
with cutaneous T-cell lymphoma, and 41% of patients with multiple sclerosis.(29)
97% of sera from homosexual men with immune thrombocytopenic purpura (ITP) and
94% of sera from homosexual men with lymphadenopathy or AIDS contain an antibody
that reacts to a p25 membrane antigen found in platelets from healthy donors and AIDS
patients, as well as a p25 antigen found in green-monkey kidney cells, human skin
fibroblasts, and herpes simplex cultured in monkey kidney cells. This reaction was absent
in sera obtained from non-homosexual patients with ITP or non-immune
thrombocytopenic purpura.(26)
35
— The p32 protein
In 1987, Henderson isolated the p30-32 and p34-36 of “HIV purified by double banding”
in sucrose density gradients. By comparing the amino acid sequences of these proteins
with Class II histocompatability DR proteins, he concluded that “the DR alpha and beta
chains appeared to be identical to the p34-36 and p30-32 proteins respectively,”(22) and
were therefore non-HIV proteins. (Class II proteins expressed on the surface of
macrophages, B-lymphocytes and activated T-lymphocytes).
An antibody test becomes meaningful only when it is standardised, that is, when a given
test result has the same meaning in all patients, in all laboratories, in all countries. From
the first antigen-antibody reactions performed by Montagnier’s(5) and Gallo’s(6) groups, it
was found that: not all the ‘HIV proteins’ react with all sera from AIDS patients or even
sera from the same patients obtained at different times; and that sera from AIDS patients
may react with proteins other than those considered to be HIV antigens.
The Western Blot (WB) test kit
In this test the ‘HIV proteins’ are dissociated and placed on a polyacrylamide gel slab.
After electrophoresis, which separates the proteins by molecular weight and charge, the
proteins are transferred to a nitro-cellulose membrane by electro-blotting. After adding
the patient’s serum to the proteins, the reaction is interpreted visually as coloured bands,
each of which is designated with a small ‘p’ and a number (p for protein and the number
is its molecular weight in kilodaltons).
In 1987 the Food and Drug Administration (FDA) licensed a WB kit manufactured by
DuPont. The DuPont kit remains the only licensed WB kit. It specifies “extremely
stringent” criteria for a positive result, namely “specific bands representing three different
gene products: p24(gag), p31(pol), and an env band, either p41, p120 or p160.”(30)
The American Red Cross defines a positive result as presence of antibodies to at least
one gene product from each of the gag, pol and env genes, without specifying which
bands.
36
The Association of State and Territorial Public Health Laboratory Directors/Department
of Defence/CDC, consider a WB positive if two out of p24, gp41 and gp120/160 are
reactive.
The Consortium for Retrovirus Serology Standardisation (CRSS) defines a positive WB
as the presence of antibodies to at least p24 or p31/32, and gp41 or gp120/160.(31)
All the other major USA laboratories for HIV testing have their own criteria.
In the scientific literature, no strips have been published of a standard positive WB. As
the instruction manual from Bio-Rad, a manufacturer of WB test kits states: “Each
laboratory performing Western Blot testing should develop its own criteria for band
interpretation. Alternatively, band interpretation may be left to the clinician.”
It is obvious that a lack of standardisation creates problems of interpretation. When FDA
criteria are used to interpret the WB, only a minimal number (less than 50%) of AIDS
patients have a positive WB. If the criteria of the CRSS are used, the percentage of
AIDS patients testing positive increases to 79%.
On the other hand the scientific data reveals major doubts about the specificity of the
proteins used as antigens for the antibody reaction. The finding that the p31/32 band
represents a cellular protein,(22) and that p120 and p160 are oligomers of p41,(32) reduces
the criteria of the CRSS and that of the American Red Cross to two bands, p21 and p41,
which are “less than perfectly specific.”(33) But even at the present, the p160, p120 and
p41 bands are considered to represent distinct viral envelope glycoproteins. The current
WHO guidelines consider a serum positive for HIV-1 antibodies if “two envelope
glycoprotein bands with or without other viral specific bands are present on the strip.”(34)
Despite this, the general consensus is that proof of the specificity of the HIV-antibody
test is firmly established.
37

Non-specific antibodies

Sick individuals with disorders of the immune system are prone to have all kinds of
antibodies that produce cross-reactions when tested with antigens for different diseases.
This is called a ‘biological false positive’ test (BFP) and is illustrated by the serological
tests to syphilis. BFPs to syphilis occur in patients with auto-immune haemolytic
anaemia, systemic lupus erythematosus (SLE), idiopathic thrombocytopenic purpura,
leprosy, and drug addiction.(35) Significantly, 14% of AIDS patients are also found to
have BFP syphilis serology.(36)
In a study conducted in 1986, 1129 serum samples from intravenous drug-users and 89
control samples from non-users were tested by two commercial ELISAs and a Western
Blot. All the samples were collected during 1971-1972. The result was that 17 of the
drug-users tested positive and all of the non-drug-users tested negative. They concluded:
“On the basis of our positive Western Blot data, it appears that parenteral drug-users
may have been exposed to HTLV-III (HIV) or a related virus as early as 1971. An
alternative but equally viable explanation is that the HTLV-III (HIV) seropositivity
detected in these specimens represents false positive or non-specific reactions.”(37)
It is known that all antibodies, including MCAs (monoclonal antibodies), are polyspecific
and are capable of reacting with immunising antigens as well as other self and non-self
components.(39, 40)
In 1980 Gallo discovered HTLV-I, which he and his associates claimed causes adult Tcell
leukaemia. Up to 25% of AIDS patients have antibodies to this retrovirus.(41)
However, AIDS patients do not develop leukaemia any more often than the general
population. This can only be interpreted as meaning either that HTLV-I does not cause
adult T-cell leukaemia, or that some retroviral antibodies detected in AIDS patients are
non-specific.
Sixty-three sera obtained from 23 patients before and immediately after immunoglobulin
(IgG) infusions were tested for HIV antibodies using WB. Of the 63 sera, 52 (83%) were
found positive. “Several samples tested in an HTLV-III (HIV) p24 radio immuno-assay
were also positive. The amount of antibody detected was greatest immediately after
infusion and decreased between infusions.”(42)
Regarding immunisation, another study involved the administration at 4-day intervals of
six 5 ml injections of Rh+ serum from a donor negative for HIV antibodies. The blood
taken from the recipient after the first immunisation was still negative to the HIVantibody
ELISA and Immunoblot assay. But after a second immunisation a weak signal
was monitored on ELISA. “After the third immunisation the signal was strong and the
38
immunoblot revealed distinct interaction with p17 and p55 proteins. An even stronger
signal was monitored after the fifth immunisation. Interaction with p17, p31, gp41, p55
and some other proteins was evident.”(43)
Individuals from the main AIDS risk groups—homosexual men, drug-users and
haemophiliacs—are exposed to many foreign substances such as semen, drugs, factor
VIII, blood and blood components, and commonly develop infections unrelated to HIV.
These individuals have high levels of antibodies directed against antigens other than HIV.
At present, evidence exists that individuals with AIDS, AIDS-related complex (ARC)
and those at risk, have immune complexes, rheumatoid factor, anti-cardiolipin, antinuclear
factor, anti-cellular, anti-platelet, anti-red cell, anti-actin, anti-DNA, anti-tubulin,
anti-thyroglobulin, anti-albumin, anti-myosin, anti-trinitrophenyl and anti-thymosin
antibodies.(44, 45)
It is also known that serum IgG levels are higher in Black blood donors than in
Caucasians.(46)
Rodriguez and his colleagues(47) found that Amazonian Indians who have no contact with
individuals outside their tribes, and have no AIDS yet, have a 3.3-13.3% HIV WB
seropositivity rate, depending on the tribe studied.
Venezuelan malaria patients were found to have a 25% to 41% positive WB result, but
no AIDS.(48)
In the light of this data it can be concluded that HIV testing is a non-specific antibody
reaction, a marker that may identify an immune disorder:
The main pillar of the HIV hypothesis is that people with AIDS have a positive antibody
reaction to the proteins of HIV. The fact that many people with AIDS test positive
shows a correlation per se, but not a causation. It is therefore an indirect test.
Examples of indirect tests:
— Cardiolipin (extract of ox heart) is used as an antigen to predict the development of
syphilis. Antibodies from a patient with syphilis react with cardiolipin, producing a
positive test. Cardiolipin antibody-reaction is an indirect indicator of the disease, but
cardiolipin is not the cause of syphilis.
— Another non-specific test is the measurement of the erythrocyte sedimentation rate
(ESR). When high, this indicates the presence and intensity of morbid processes within
the body, and has the capacity to predict a likelihood of death within the next several
years far above a normal ESR.
39
An HIV-positive test is an evidence of the result of the disease, not of the cause of the
disease.

PCR and viral load

These very specialised laboratory tools are used to indirectly confirm viral presence and
replication. As indirect tools they have the same problem as the previous ones if the
diagnosis of HIV is based on their results.
Polymerase chain reaction (PCR) is a very specialised laboratory technique by which
sequences of DNA or RNA found in tissues can be amplified by the use of primers from
DNA or RNA of the same type of tissue.
Primers claimed to represent segments of RNA or its complementary DNA (cDNA) from
HIV are used to amplify similar sequences found in the tissues of AIDS patients.
Having seen the way in which HIV has been ‘isolated’, there is no real proof that the
RNA of the primers used in the PCR test are constituents of a viral particle. Endogenous
sequences could be the source of these bits of RNA. Therefore, transcriptional activities
of endogenous sequences must be considered.
Humans are born with DNA nucleotide sequences known as endogenous retroviral
sequences. Unlike genomes of bacteria, viruses other than retroviruses and other
infectious agents, which if present in humans are clearly exogenously acquired, retroviral
RNAs (proviral DNAs) are present in all of us and are known to constitute at least 1% of
the human genome.(141) When expressed, these DNAs give rise to retroviruses known as
endogenous retroviruses.
With regard to the HIV viral load tests, which are used to quantify HIV in plasma,
researchers from the Massachusetts School of Medicine expressed the problem
concisely: “Plasma viral [RNA] load tests were neither developed nor evaluated for the
diagnosis of HIV infection. Their performance in patients who are not infected with HIV
is unknown, and their use leads to mis-diagnosis of HIV infection.”(141)
According to the manufacturer Roche: “The Amplicor HIV-1 [RNA] monitor test is not
intended to be used as a screening test for HIV-1 or as a diagnostic test to confirm the
presence of HIV-1 infection.” (Roche Diagnostic Systems, 06/96, packet insert)
40

C) IMMUNE DEFICIENCY

Immune deficiency is a pivotal aspect of the theory of HIV-AIDS, because it is the
expression of the cytopathic action of the virus. The destruction of the T CD4+
lymphocytes causes a depletion of a very important part of the immune defence
mechanism. Cell mediated immune deficiency leaves the host open to infections by
intracellular pathogens and capsulated bacteria. Immune deficiency is the source from
which the vast array of 30-odd diseases springs.

Lymphocytes and immune responses

Human immune response is carried out by a group of blood cells called leukocytes or
white cells. Lymphocytes are a type of these. Lymphocytes are the effector cells for
immune responses to immunogens, that is, to materials not recognised as ‘self’ and
therefore triggering reactions designed to neutralise or destroy ‘non-self’. Immune
responses combat the invasion of the body by organisms, cause the rejection of organ
transplants between individuals with different histocompatibility antigens, and may also
suppress the growth of malignant cells.
There are two types of immune responses: cell-mediated and antibody-mediated.
Cell-mediated response means that the immune cells kill off bacteria directly by
phagocytosis. This kind of response is carried out by a type of white cell called
granulocytes (neutrophils, eosinophils and basophils) and monocytes (macrophages).
They come from a common myeloid stem cell in the bone marrow.
Antibody-mediated response means that for the immune cells to react, they need a
recognition of the target first, and that is facilitated by an antibody. This very specific
response is the action of lymphocytes and macrophages (monocytes).
The lymphocytes arise from a lymphoid stem cell in the bone marrow and are further
processed into immunologically competent cells in the thymus (T-cells) and bone marrow
(B-cells). They are of three functional classes: T-lymphocytes (T-cells), B-lymphocytes
(B-cells), and a small group called natural killers (NKs).
We are interested in T-lymphocytes, which regulate and mediate immune reactions and
also regulate antibody synthesis.
In our cells, a group of genes from chromosome 6 produce two types of molecules that
show on the surface of the cell as the ‘ID’ of the cell. These are named Class I and Class
41
II molecules (major histocompatibility complex). These molecules are the tissue blueprint
of an individual and largely determine whether organ or tissue transplants are
recognised as self or foreign and, therefore, accepted or rejected. Class I molecules are in
the surface membrane of most of the nucleated cells, Class II molecules are expressed
normally by only a few cell types: hemopoietic progenitor cells, B-lymphocytes,
macrophages and activated T-lymphocytes.
T-lymphocytes possess a cell surface T-cell antigen receptor, with the capacity to
distinguish between non-self and self Class I and II proteins (MHC). This receptor
contains a molecule, CD3+, which all mature T-cells posses. As a means of identifying
mature T-lymphocytes in tissues and body fluids, monoclonal antibodies have been
developed that recognise CD3+. The binding of the antibody to the CD3+ molecule is
used as the counting tool for mature T-lymphocyte population.
While being processed by the thymus, T-cells also acquire surface glycoprotein
molecules that determine whether the antigen receptor on the surface of the T-cell will
react with an antigen of Class I or II molecules.
With monoclonal antibodies, two such surface glycoproteins can be identified, CD4+ and
CD8+. CD4+ T-cells recognise Class II molecules, and CD8+ T-cells recognise Class I
molecules.
T4 lymphocytes, or helper cells, activate macrophages to destroy affected cells and also
B-lymphocytes to secrete immunoglobulins, and induce all lymphocyte sub-populations
to proliferate.
T8 lymphocytes, suppresser cells, suppress the proliferative response of other T-cells and
of B-cell immunoglobulin production and secretion. T8 suppresser cells keep the immune
responses from going out of control.
The T4 lymphocyte is the agreed target of HIV. The progressive destruction of T4 by
HIV reduces the capacity of the immune system to respond to other immune attacks. The
immune deficiency then allows the development of a diversity of diseases, and although
most of them are not fatal, the patient eventually dies from them.

The CD4+ T-lymphocyte cell count — T4/T8 cell ratio

In the 1970s it was known that patients who were treated with immune-suppressive
drugs, or who suffered from ‘immune-suppressive illnesses’, had relatively high
frequencies of malignancies and opportunistic infections (OIs).
42
Following the frequent diagnosis of Kaposi’s sarcoma (KS) and OIs among homosexual
men, intravenous drug-users and haemophiliacs, it was realised that when T-lymphocytes
from these patients were reacted with monoclonal antibodies (MCA) to the CD4 antigen,
the number of CD4 antigen-bearing cells diminished. For that reason it was thought that
the high frequency of these diseases in these groups was due to the death of T4-cells and
was the direct result of suppressed cellular immunity defined by diminished numbers of
T4 helper lymphocytes. The newly postulated Acquired Immune Deficiency Syndrome
(AIDS) was defined in 1982 by the Centres for Disease Control (CDC) as “illnesses in a
person who:
1. Has either biopsy-proven KS or culture-proven life-threatening OI;
2. Is under the age of 60;
3. Has no history of immune suppressive underlying illness or immune suppressive
therapy.”
Then, in 1984, Gallo and his colleagues claimed that AIDS was caused by the HIV
retrovirus. It was postulated that HIV is a cytopathic retrovirus and causes immune
deficiency by destroying T4-cell (helper) lymphocytes. The destruction of T4
lymphocytes is necessary and sufficient for the appearance of the clinical syndrome.
The technology for counting T-cells appeared in 1980. According to the HIV theory of
AIDS pathogenesis, “The Human Immune deficiency Virus (HIV), the etiologic agent of
the Acquired Immune Deficiency Syndrome (AIDS), has the capability of selectively
infecting and ultimately incapacitating the immune system. HIV-induced immunesuppression
results in a host defence defect that renders the body highly susceptible to
‘opportunistic’ infections and neoplasms.”(97) Lower counts of T4 lymphocytes were
reported in AIDS patients and currently the selective depletion of CD4-bearing
helper/inducer lymphocytes has become the hallmark for the assessment of active AIDS.
Decrease of T4-cells to approximately 200 x 106/l leads to the development of
‘constitutional symptoms’, and less than 100 x 106/l to opportunistic diseases.(98)
However, neither Montagnier nor Gallo in any of their papers were able to present any
proof of such cytopathic action.(5, 6)

The in vitro tests

Most of the hypothesis of how the virus acts has been drawn from experimental in vitro
tests, in a laboratory test tube.
43
In a paper from 1986 Montagnier wrote, “Replication and cytopathic effect of LAV [the
French name for HIV] can only be observed in activated T4-cells [meaning T4-cells that
have been immunologically stimulated]. Indeed, LAV infection of resting T4-cells does
not lead to viral replication or to expression of viral antigens on the cell surface [no HIV
proteins], while stimulation by lectins or antigens of the same cells results in the
production of viral particles, antigenic expression and the cytopathic effect (cell
death).”(72)
In trying to prove how the action of HIV could account for the decrease of T4-cells, a
hypothesis was put forward in 1991 of a “single unique mechanism, activation-induced
T-cell death (programmed cell death, PCD, or apoptosis) that can account for both the
functional and numerical abnormalities of T4-cells in HIV infected patients.”(71) In
support of their theory they reported that stimulation of peripheral blood mononuclear
cells of asymptomatic HIV infected individuals with pokeweed mitogen or
staphylococcal enterotoxin B was followed by cell death, whereas no death was observed
at 48h in the unstimulated cells. Death was only observed in the CD4+ enriched
population and not in the CD8+ lymphocytes.
So, in order to produce an experimental model of what the HIV virus might be doing to
T4-cells, all the experiments absolutely required an immunological stimulation in order to
induce cell death.
Up until 1991 very little was presented regarding the effects of the laboratory activating
agents themselves on cell survival. However, Montagnier and his colleagues showed in
1990 that activation, in the absence of HIV, can induce the same cytopathic effects.(73) If
this shows that HIV is neither necessary nor sufficient for the induction of cytopathic
effects observed in the experimental model of HIV infected cultures, these cytopathic
effects are most likely to be caused by the many activating agents to which the cultures
are exposed.
Activation (stimulation) is induced by oxidation. Evidence shows that oxidising agents,
including all mitogenic (activating) agents, can induce: reversible cellular changes,
cellular activation, malignant transformation, mitogen unresponsive cells, and cellular
death, including death by apoptosis.(74)
Apoptosis occurs under both healthy and pathological conditions, is frequently prominent
among the proliferating cells of lymphoid germinal centres, and can be enhanced by
numerous agents including radiation, cytotoxic drugs, corticosteroids and calcium
ionophore A23187. Apoptosis is cellular death characterised by morphological criteria:
cellular condensation, DNA fragmentation, and plasma membrane ‘blebbing’ leading to
the release of ‘apoptic bodies’ which vary widely in size and some of which contain
44
pyknotic chromatin (genetic material) surrounded by intact membranes.(75-78) These
changes are induced by increased concentration of Ca+++, which in turn induces
contraction of the cytoskeleton, whose main components are the proteins actin and
myosin.(79-83) Intracellular free Ca++ concentration is regulated by the cellular redox state.
Oxidation leads to an increased and reduction to a decreased Ca++ concentration.(84)
Cellular surface blebbing, chromatin condensation and apoptosis are the direct result of
cellular oxidation in general and of cellular sulphydryl groups in particular. In a paper
from 1992, Montagnier explains how an anti-oxidant prevents apoptosis and early cell
death in lymphocytes from HIV infected individuals.(85)
From another test-tube model, suspicions can arise about the cytopathic action of HIV,
meaning the effect that HIV has on the cells that it is cultured in. The H9 clone is widely
used, in both research and commercially, for producing what is regarded to be the HIV
proteins used in antibody-test kits. What is interesting in this case is that although HIV is
thought to kill T4-cells, the leukaemic cell line, as well as its H9 clone in which the HIV
is grown, do not exhibit any cytopathic effect from HIV, in fact both are immortal even
when infected with HIV. So these cells allow what is believed to be HIV to grow
indefinitely. The proteins produced from these cells are the ones patented by R. Gallo as
the antigens for testing antibody reaction. All the test kits for HIV come from these
proteins.(110, 111)

Immune suppression and antigenic stimulation

In 1985 Montagnier wrote: “The clinical AIDS syndrome occurs in a minority of infected
persons, who generally have in common a past of antigenic stimulation and of immune
depression before LAV [HIV] infection.”(86) This means that in the AIDS risk group,
acquired immune deficiency appears before the ‘HIV infection’, before testing ‘positive’.
In another paper from 1991, Montagnier and colleagues showed that in acutely HIV
CEM cultures, in the presence of mycoplasma removal agent, cell death (apoptosis) was
maximum at 6-7 days post-infection, “whereas maximal virus production occurred at 10-
17 days.”(87) That is, maximum effect precedes maximum cause.
A study of intravenous drug-users in New York showed that “the relative risk for
seroconversion among subjects with one or more CD4 count below 500 cells/ul,
compared with HIV-negative subjects with all counts above 500 cells/ul, was 4.53.”(88) A
similar study in Italy showed that “a low number of T4-cells was the highest risk for HIV
infection.”(89) The decrease in T4-cells is the risk factor for seroconversion and not vice
45
versa, and therefore factors other than HIV lead to both T4 decrease and ‘HIV positive’
tests.
Data presented from the Multicenter AIDS Cohort Study (MACS 1993) shows that HIV
seropositive homosexual men at least 1.67 to 3.67 years prior to a clinical diagnosis of
AIDS, as well as HIV seronegative homosexual men—although the frequency in the
latter is lower—suffer from a wide variety of complaints including fatigue, shortness of
breath, night sweats, rashes, coughs, diarrhoea, headaches, thrush, skin discoloration,
fever, weight loss, sore throats, depression, anaemia and sexually transmitted
diseases.(100) Some of the diseases that occur in these individuals, or the agents that cause
them, including EBV and CMV, are immune-suppressive. Many of the agents used in
treatment, including corticosteroids and some antibiotics, as well as recreational drugs
like cocaine, heroin and the wide-spread use of amyl nitrite, are also known to be
immune-suppressive.
Very important to the pathogenesis of AIDS is the homosexual practice of anal
intercourse, regarded as immune-suppressive due to the oxidative effect of semen that
brings foreign proteins directly into the blood stream by rectal absorption. The critical
structural difference between the epithelium of the rectum and vagina reveals how
biologically unnatural anal intercourse is. The vagina is lined with a thick stratified
squamous epithelium that makes ulceration and penetration of semen into the vascular
lamina unlikely. In contrast, semen in the rectum is separated from blood vessels and
lymphatics by a single layer of cells that is easily penetrated and ulcerated during anal
intercourse.
Studies of haemophiliacs receiving factor VIII, and by that token known to be exposed
to immune-suppression, concluded: “We have thus been able to compare lymphocyte
subset data before and after infection with HTLV-III (HIV). It is commonly assumed
that the reduction in T-helper cell numbers is a result of the HTLV-III (HIV) virus being
tropic for T-helper cells. Our finding in this study that T-helper cell numbers and
helper/suppresser ratios did not change after infection supports our previous conclusion
that the abnormal T-lymphocyte subsets are a result of the intravenous infusion of factor
VIII concentrates per se, not HTLV-III (HIV) infection.”(101)
In the light of the above studies, an immune-suppressive action on the immune system,
by whatever means, and not HIV, is more likely to be the cause of the depletion of T4-
cells and the cause also of the posterior seropositive conversion (HIV+ test), which in
fact is a non-specific antibody marker for a particular immune disorder.
“In TB as well as in lepromatous leprosy, an immune-suppressive state will
frequently develop in the host. This state is characterised by T lymphopenia
46
with a decreased number of T-helper cells and an inverted T-helper/Tsuppresser
cell ratio. [...] Immune-suppression induced by the infection with
M tuberculosis can persist for life, even when TB is not progressive.”(96)
Patients who have malaria have severe immunoregulatory disturbances including a
decrease in T4-cells. A significant number of these patients also test positive for HIV but
they do not develop the AIDS clinical syndrome, so “exposure to HTLV-III/LAV (HIV)
or related retroviruses and the occurrence of severe immunoregulatory disturbances may
not be sufficient for the induction of AIDS.”(99)
On the other hand, many HIV-positive individuals continue to have normal T4-cell
counts years after the seroconversion.(90) Most of these individuals remain healthy. In
these cases the ‘positive’ test is another example of antibody cross-reaction.

T4/T8 ratio

T-cells are lymphocytes produced by the thymus. They are part of what is called the cellmediated
immune response. T4+ T-cells provide helper functions for optimal
development of cytotoxicity in cell-mediated lympholysis. In addition, the T4+ subset
produces a variety of helper factors that induce B-cells to secrete immunoglobulin and all
lymphocyte sub-populations to proliferate. T8+ T-cells suppress the proliferative
response of other T-cells, and B-cell immunoglobulin production and secretion.
From the beginning it was realised that in AIDS patients the decrease in T4 lymphocytes
is accompanied by an increase in T8 lymphocytes, “with kinetics that mirrored the loss of
CD4+ cells, resulting in a CD8 polarisation,”(91) while the total T-cell population remains
relatively constant. There is an interesting explanation which reveals that the “loss of
either CD4+ or CD8+ T-cells is detected by the immune system only as a decrease in
CD3+ T-cells (as total mature T-cells). The compensatory response to such a selective
decrease, then, is to generate both CD4+ and CD8+ T-cells in order to bring the total
CD3+ T-cells back to a normal level. The consequence of this non-selective T-cell
replacement after a selective depletion of one T-cell subset would be an alteration in the
CD4 to CD8 ratio after normalisation of the total T-cell count with a polarisation
towards the subset that had not been initially depleted. [...] Repeated events of selective
CD4+ T-cell killing will result in higher and higher CD8+ T-cell counts and lower and
lower CD4 T-cell counts.”(91-93)
Knowing that T4 and T8 cells are identified and counted among the T-cell population by
the expression of their surface antigens, which are molecular markers of differentiation,
47
there have been a number of studies showing that in vitro stimulation of T-cells by PHA,
ConA, radiation PMA and polybrene, all of which are oxidising agents, leads to a
possible change of phenotype (change of the type of protein on the T-cell surface). The
experiments(94, 95) recorded antigenic shifts between T4, T8 and T10. So it can be argued
that in vivo, due to the exposure of AIDS risk groups to many oxidising agents and well
known mitogens, the selective decrease of T4 and the increased proliferation of T8 cells
may not be the result of the destruction of the T4 subset, but of a loss of T4 surface
markers and an acquisition of T8 surface markers.

From evidence to proof

It is necessary to point out that all the above evidence comes from laboratory counting
devices and procedures. But, in the case of AIDS, these laboratory tools only produce
indirect evidence and are therefore non-specific. The evidence is circumstantial, and
cannot be taken as a means of discrimination. We are not saying that the counting is not
accurate, but it tells us nothing about the identity of what is being counted.
When a phenomenon can be produced by different causes, in order to know with
certainty which one of them is responsible, we need procedures that can reflect direct
and therefore specific characteristics of the phenomenon to leave no doubt as to its
cause. Only then does the evidence become proof.
Herein lies the problem, because in the case of HIV-AIDS, all of these accurate indirect
methods are used for direct identification of HIV. By bypassing the standard method of
identification with Gallo’s short-cut, the electron micrographs become irrelevant because
they do not reveal the identity of what is depicted per se. Reverse transcription is
meaningless because it is not exclusive to retroviruses and therefore is not an
identification of them. HIV proteins might not be viral proteins, but rather cellular ones,
and are therefore no proof of a virus, nor does the positive HIV-test made with these
proteins constitute proof. Antibody lymphocyte counting of the CD4+ subset is an
indirect method of counting T-cells, and becomes even more indirect when the counting
is done under conditions of immune-suppression—that is, while the patient is under
immune suppressive drugs or practices.
These laboratory procedures are biological amplifiers of microscopic aspects of life, but
not like a magnifying glass or microscope. Their amplification is ‘blind’ because it only
signals that certain reactions are taking place. Their answer is not specific, so we cannot
ask them. All of the procedures of HIV identification are in themselves not direct or
specific proof of HIV, and are therefore irrelevant as a means of diagnosis.
48

D) SEXUAL TRANSMISSION

Besides blood transfusion, infected intravenous needles and mother-to-child
transmission, sexual transmission is considered to be the main mechanism of infection.
In the mid 1970s, sexually transmitted diseases (STDs) were rising at a terrifying rate
among homosexual groups in many cities of the USA and Europe, with an alarming
increase in gonorrhoea and syphilis. Promiscuity meant continuous re-infection, for
which continuous antibiotic treatment as a prophylaxis was the norm. But parasitic
infections were also appearing, as were persistent fevers, swollen lymph glands, chronic
skin eruptions, and multiple viral infections (CMV) that would not clear up.
One of these diseases was the particular parasitic disease pneumocystic pneumonia,
caused by the pneumocystis cariini. This is relevant because it normally only occurs as a
complication produced by the use of chemotherapy to suppress the immune system in the
treatment of leukaemia in children (ATL). It led to the suspicion that an immune
deficiency could be behind the problem. In 1981, for the first time, blood from 30
homosexual men was tested with the newly emerging technique of T-cell counting, by D.
Purtillo, a pioneer of the technique at the University of Nebraska. Ten among the 30 had
extremely low counts. A blind test correlated the 10 men with a low T-cell count to high
promiscuity, in comparison with the other 10 with ‘monogamous’ relationships and
normal T-cell counts (Lancet, 1982). Promiscuity was depressing the immune system.
Epidemiological studies show that the clusters of cases of pneumocystic pneumonia had
in common that they occurred in big cities (New York, Los Angeles, and San Francisco),
that all were young male, very promiscuous homosexuals involved in the long-term use
of antibiotics for their shared tendency to contract venereal diseases, and chronic users of
nitrite inhalant and other recreational drugs for sexual stimulation.
Another of the particularly rare features of the collapse of the health of the people
involved in these sexual practices was a rare form of cancer, Kaposi’s sarcoma, only
observed before in old men, that was now appearing among young men, and particularly
affecting the lungs. Cancer researchers looking for viruses that could transmit cancer had
spotted the new candidates for their oncoviral theory. The lymphocytes of these patients,
they believed, must contain retroviruses. After the ‘identification’ of HIV, the now
leading HIV-experts (formerly cancer research experts) required a means of transmission
for the virus.
49
Sex, or to be more precise anal sex, seems to be the common link between these people.
If we then introduce the idea (1984) of a virus, the equation is closed: sex must be the
transmission mechanism.
The next step is to prove that heterosexual transmission is possible. However, there is no
direct proof of it. There is not one single study from any country proving sexual
transmission of HIV based upon evidence of HIV in genital secretions. Studies where
attempts are made to prove a correlation between HIV in the blood and in genital
secretions indicate that approximately 85% of male and 80% of female genital secretion
samples obtained from HIV-positive subjects do not harbour HIV.(128)
The only evidence said to prove heterosexual transmission is epidemiological, meaning
the correlation of seropositivity and sexual behaviour.
The male homosexual group accounts for 2/3 of all the male AIDS cases in the USA and
Europe (90% of all AIDS cases are men). The heterosexual group in the AIDS statistic is
made up of the remaining 1/3 of the male cases who are not homosexual, and by women
(10% of all AIDS cases are women). Almost all the non-homosexual men in the group
are intravenous drug-users, alongside a small number of haemophiliacs. Almost all the
women are intravenous drug-users. Yet all these cases have been classified for statistical
purposes as heterosexually transmitted for the simple reason that they happened among
heterosexual people.
The largest study of female sexual partners of HIV-positive haemophiliacs was
conducted between August 1985 and February 1989 by the U.S. Transfusion Safety
Study Group. The researchers followed up 151 females HIV negative at the beginning of
the study. None became HIV positive despite the fact that 13 of the 151 women became
pregnant.(140)
The infective capacity of AIDS and its transmission are more an assumption than a
proven fact. Doctors are at risk of contracting AIDS from patients, HIV researchers
from virus preparations, wives of HIV-positive haemophiliacs from husbands, and
prostitutes from clients. But in the peer-reviewed literature there is not one doctor or
nurse who has ever contracted AIDS (nor HIV) from over 816,000 AIDS patients
(deaths) recorded in the USA in 22 years (Centres for Disease Control and Prevention
2001). Not one of over ten thousand HIV researchers has contracted AIDS. Wives of
haemophiliacs do not get AIDS. And there is no AIDS epidemic among prostitutes,
except among intravenous drug-users.(106)
The longest and best study to prove that HIV is heterosexually transmitted, was a 10-
year study in northern California completed in 1997.(112) Their findings showed:
50
The risk factors for seroconversion (becoming positive) were:
- Anal intercourse;
- Having partners who acquired this infection through intravenous-drug use;
- The presence in the females of STDs;
- They estimated that the likelihood of female-to-male transmission was 8
times lower than male-to-female;
- They estimated that the risk to a non-infected male of acquiring HIV
infection from his infected female partner per contact is 0.00011 (1/9000).
This means that on average, males having sexual intercourse daily with an infected
partner for 16 years (that is 6000 contacts at 365 per year), would score a 50%
probability of becoming infected. But if sexual intercourse takes place once a week it
would take 115 years to reach the same probability.
Under such circumstances, one must question how HIV could spread to epidemic
proportions as the result of bi-directional heterosexual transmission. And yet the claimed
mechanism of heterosexual transmission is said to be at the core of the present AIDS
epidemic that is ravaging Africa.

E) MOTHER-TO-CHILD TRANSMISSION

At the end of 1997 the World Health Organisation reported an estimate of 1.1 million
children living with human immunodeficiency virus (HIV) infection world-wide. Of
these, the great majority lived in sub-Saharan Africa and were infected by their mothers
during pregnancy, delivery or breast-feeding.
The CDC 1994 Revised Classification System for HIV Infection in Children under 13
years of age, explains that “the diagnosis of HIV infection in children born to HIVinfected
mothers is complicated by the presence of the maternal anti-HIV IgG antibody,
which crosses the placenta to the foetus. Virtually all these children are HIV-antibody
positive at birth, although only 15% to 30% are actually infected. In uninfected children,
this antibody usually becomes undetectable by 9 months of age but occasionally remains
detectable until 18 months of age. Therefore, standard anti-HIV IgG antibody tests
cannot be used to indicate reliably a child’s infection status before 18 months of age.
Polymerase chain reaction (PCR) and virus culture are probably the most sensitive and
specific assays for detecting HIV infection in children born to infected mothers.”
51
To prove that mother-to-child transmission of HIV takes place, one must first have proof
that HIV exists. At present, infection of the mother is determined by antibody tests and
that of the child by an antibody test, ‘HIV isolation’ and measurements of HIV-RNA or
DNA utilising the polymerase chain reaction (PCR). However, due to the poor
infrastructure of many African Health Services and the high cost of laboratory
techniques, the Bangui AIDS Definition for children in Africa was drawn. This definition
gives clinical criteria to be applied in order to diagnose children infected with HIV by
transmission from their mothers without any laboratory tests. In much of the African
epidemiological data on children infected with HIV, the infection is solely diagnosed by
the satisfaction of clinical criteria.
According to the WHO, a minimum of 330,000 and a maximum of 670,000 children in
the world died from AIDS in 1999. The WHO estimates as follows:
- Australia and New Zealand had under 100 cases in 1999. By September
2000, 32 deaths from AIDS in children had been recorded in Australia.
- Canada, under 100 deaths in 1999.
- United States, minimum 250 and maximum 380 AIDS deaths in children
during 1999. The cumulative total of child deaths from AIDS in the USA up
until June 2000 is 8804.
- No estimated deaths from AIDS in children are reported from Western
Europe, Eastern Europe or Central Asia, nor from North Africa or the
Middle East.
- Ethiopia, estimated 35,000 to 91,000 deaths in 1999.
- Nigeria, estimated 41,000 to 64,000 deaths in 1999.
- South Africa, estimated 36,000 to 74,000 deaths in 1999.
- Uganda, estimated 18,000 to 32,000 deaths in 1999.
Although the estimated deaths in Africa, especially in sub-Saharan Africa, are high, they
are only estimates.
According to the WHO there are 300-500 million clinical cases of malaria each year and
more than 90% of all cases occur in sub-Saharan Africa. Most of the 1-3 million who die
from malaria are children, mainly in Africa, in which malaria is hyper-endemic. The
mortality rate is highest during the first two years of life.
In the WHO 2000 report we read: “Diarrhoea is the leading cause of illness and death
among children in developing countries, where an estimated 1.3 thousand million
episodes and 4 million deaths occur each year in under-fives. Worldwide, these children
experience an average of 3.3 episodes a year, but in some areas the average exceeds nine
episodes each year. Where episodes are frequent, young children may spend more than
52
15% of their days with diarrhoea. About 80% of deaths due to diarrhoea occur in the
first two years of life.”
The diseases from which HIV-infected children die are the same diseases from which
non-infected children die. In particular, African HIV-infected children die from the
common causes in that continent: tuberculosis, diarrhoea, pneumonia and malnutrition.
A paper entitled ‘Severe malnutrition and paediatric AIDS: a diagnostic problem in rural
Africa’ published in 1988(130) reported the Ivory Coast’s morbidity among HIV-positive
and HIV-negative malnourished children. The study was about 94 children, of which 30
were HIV-positive and 64 HIV-negative. 90% of them suffered from severe malnutrition
(weight less than 60% of the expected weight for their age).

Disease HIV-positive 30 of 94 HIV-negative 64 of 94

Chronic diarrhoea 26 (87%) 43 (67%)
Generalised lymphadenopathy 22 (73%) 34 (53%)
Oropharingeal candidiasis 20 (67%) 34 (53%)
Prolonged fever 19 (63%) 21 (33%)
Persistent cough 12 (40%) 13 (20%)
Generalised dermatitis 4 (13%) 6 (9%)
The signs and symptoms which are considered to signify death from AIDS in the Bangui
definition, or the latest CDC definition, are those of tuberculosis, malaria, gastrointestinal
parasitic infections, and malnutrition. With clinical criteria only, it is not possible to
distinguish between death from AIDS or other common African diseases.
The following data is from the Survey of Race Relations in South Africa. It illustrates the
distribution of the African AIDS-defining disease of tuberculosis (50% of all AIDS cases
are TB), and its increase in certain groups and decrease in others according to race, long
before the AIDS era:

Tuberculosis: reported cases 1951 (whole country)

Africans Whites Coloured Asian
19,392 1477 4586 1084
53

Tuberculosis: reported cases 1968

Africans Whites Coloured Asian
61,292 921 7,481 990

Infant mortality per 1000 live births, in 1953/54

Africans Whites Coloured Asian
210 33 134 66
The term ‘protein-energy malnutrition’ covers the spectrum of clinical conditions seen in
children and adults due to under-nourishment. Severe starvation leads to a clinical
feature called Kwashiorkor which occurs typically in a young child displaced from
breast-feeding by a new baby, and fed a diet with a very low protein content. Apathy,
anorexia, generalised oedema, with skin pigmentation and thickening, distended abdomen
due to hepatomegalia and/or ascites—reminiscent of the frequent images seen on
television of starving children with big bellies. Protein-energy malnutrition leads to a
depression of the immunological defence mechanism, resulting in a decreased resistance
to infection.(131)
From the same Survey by the Institute of Race Relations, a distribution of reported
Kwashiorkor cases among races from 1964/65 shows:
Africans Whites Coloured Asian
13,358 Zero 410 40
One last piece of data from the same Survey shows the percentage of children under 12
years of age with stunted growth (including Kwashiorkor) from 1988:

South Africa Neighbouring countries

Eastern Cape 58% Mauritius 21%
Northern Cape 80% Swaziland 10%
Transvaal 49% Zambia 19%
“It is important to appreciate that even if the highest [30%] current
prevalences of HIV-1 in Africa were found among all women of childbearing
54
age, HIV would still only account for a minority of child deaths and rank
some way behind mortality associated with respiratory tract infections and
diarrhoeal diseases. Similarly, HIV is not the only prevalent lethal congenital
infection. Syphilis is a massive source of foetal wastage and infant death in
Africa. Our calculations suggest that the HIV-1 epidemic is unlikely to
overwhelm most existing differentials between African countries in the level
of child mortality. Countries with relatively low child mortality in the 1980s
are likely to remain so in the future.”(139)
The biggest epidemic in Africa is poverty. Malnutrition is the principal factor responsible
for immune deficiency among the African people. The epidemiological race distribution
of the diseases is none other than poverty distribution, as the South African figures of TB
in the 50s and 60s show. Poverty is also the common denominator among the mothers
that supposedly transmit HIV to their children in the U.S./Europe AIDS epidemic.
Looking at epidemiological data from the U.S. AIDS epidemic in children, the first
feature to appear is again racial distribution. With negligible exceptions, the children who
are said to have been infected by their mothers are Black and to a lesser extent Hispanics,
that is, these are children born to poor women. According to Dr. H Gayle, Director of
the National Center for HIV, STD and TB Prevention (CDC), in 2000: “In the United
States, of all the AIDS cases reported in children, 17% are white, 58.6% black, 22.9%
Hispanic and the rest other minorities.”(129) The race factor of the epidemic is none other
than that of poverty.
In all of the U.S. studies reporting evidence of mother-to-child transmission, over 2/3 of
the mothers are intravenous drug-users. Maternal drug abuse is one of the main factors
responsible for pre-term delivery and low birth weight. The studies from the USA show
that children of drug-using or economically disadvantaged mothers are of low birth
weight, and develop immune deficiency and a range of diseases.(133) Immune deficiency
and illness in Black and Hispanic children are related to parenteral drug use by the
mothers, neglect, and malnutrition.(134) In the studies of positive PCR in children with or
without AIDS, all the children are born to socio-economically disadvantaged, drugaddicted
mothers.(135)
In the USA, the evidence on which the conclusion of what is called vertical transmission,
mother-to-child transmission, is based, is from studies of drug-addicted mothers and
prostitutes whose immune-suppressed infants suffered from recurring viral and fungal
infections and died from pneumocystis carinii pneumonia.(136)
55
In the European studies, “most of the children were born to mothers who abused
intravenous drugs. As well as exposure to intra-uterine HIV infection, these infants are at
increased risk of other congenital infections, low birth weight, neurological disorders
resulting from drug withdrawal, and other perinatal problems. The observed excess
perinatal mortality is probably due to the background of drug abuse as demonstrated by
the association between low birth weight and drug abuse during pregnancy, rather than
being an effect of HIV infection alone. In many cases social deprivation is encountered
after birth, which can adversely affect the child’s development and health.”(132)
All of these infants from Africa, the USA and Europe whom we see classified in AIDS
statistics as infected by HIV, have in common immune deficiency. The African children
develop the immune deficiency from malnutrition; in the USA and Europe it is caused by
immune-suppression from intravenous drug abuse (heroine, cocaine, amphetamines) by
the mothers during pregnancy, and malnutrition.
All of the children in all of the studies are from disadvantaged mothers.

Breast-feeding and transmission of HIV

There is unquestionable evidence that breast-feeding protects babies against morbidity
and mortality from infectious diseases. It provides ideal nutrition to the infant at no cost
and gives an immunological protection against agents responsible for diarrhoeal and
respiratory diseases, as well as other infections.
Regarding the isolation of HIV in breast milk, from 1985 until the present, only two
publications can be found. After scrutiny, neither of them shows any direct proof of the
isolation of HIV in milk. Indirect reverse transcriptase activity, reaction with rabbit
hyper-immune serum against HIV, but no direct isolation of HIV. In neither paper did
the author have any experimental controls, nor any comparisons with non-HIV
mothers.(137)
Posterior studies have been done with PCR, amplifying what is thought to be HIV-RNA.
But again this is an indirect method of identification since there is no real proof of the
identity of what is being amplified.(138)
In the case of children with AIDS, the positive HIV test is completely irrelevant because
the antibodies can come from the mother and not from the child, as the above 1994 CDC
classification advises. So an HIV-positive test is no evidence of mother-to-child
transmission before 18 months of age. Therefore, if the diagnosis has to be drawn from
clinical criteria, and immune deficiency in children can be caused by factors other than
56
HIV—immune-suppression by intravenous drug abuse and immune-depression by poor
protein-calorie intake—there is no way that we can distinguish, on clinical grounds,
between an immune deficiency produced by immune-suppression, from one produced by
malnutrition, and one produced by HIV. One is forced to wonder just how misleading all
the statistical data about HIV-infected children might be.
The real meaning of the diagnosis of mother-to-child transmission is the therapeutic
indication for the anti-retroviral drugs AZT and Nevirapine.
A particularly interesting and thorough study on the evidence regarding AZT and
Nevirapine and mother-to-child transmission has been conducted by a brilliant group of
scientists from Perth, Western Australia.(146) One of them, E. Papadopulos-Eleopulos,
has also been responsible for one of the most scientifically elegant explanations of
immune deficiency by the oxidative effect of immune suppressants.(23)

F) AIDS IN AFRICA

AIDS in Africa is almost unrecognisably different from AIDS in the USA and Europe.
As mentioned before, 90% of AIDS victims in Europe and America to this day are males
between 20 and 50 years of age. A third of these males are intravenous drug-users, and
use those drugs for years at a time, and two-thirds, approximately, are male
homosexuals. The remaining approximately 10% identified as AIDS risk groups are
haemophiliacs, transfusion recipients, and females, almost all of whom are intravenous
drug-users.
Regarding the heterosexual transmission hypothesis, the definition that in Africa the HIV
virus is transmitted by heterosexual relationships is based simply on the striking fact that
the syndrome in Africa exhibits a gender ratio between men and women of 1:1, whereas
in the West it is 15:1.(64, 66) While this hypothesis is awkward in the USA and Europe,
due to the distribution of 90% men and 10% women, in Africa the viral theory fits the
pattern of an infectious transmitted disease by striking at random, affecting equally both
sexes. It is, undeniably, very difficult to scientifically explain how a virus can behave so
differently depending on geographical location, so much so that a person becoming
infected in a Western country has a 1 in 15 chance of being a woman, while in Africa it is
50-50%.
The other striking feature about the sexual dimension of HIV is that in non-African
countries, the only sexual practice leading to an increased risk of becoming HIVantibody-
positive is anal intercourse(68, 69, 70)—which is almost a non-practice among
57
native Africans. So HIV, like pregnancy, can only be acquired by the passive sexual
partner and cannot be transmitted to the active partner. In the whole history of medicine
there has never been an example of a sexually transmitted disease that is spread unidirectionally,
and certainly not one that is spread uni-directionally in one country and bidirectionally
in another.
AIDS researchers in Africa, including those from the CDC and WHO, admit that clinical
symptoms similar to AIDS and wide-spread immune deficiency has existed in Africa for a
considerable time and that this has not been due to HIV.

Clinical symptoms of the African AIDS

Unlike the AIDS definition in the West, the World Health Organisation’s Bangui
Definition for Africa does not require immunological (T4 count or antibody+) tests or a
specific disease diagnosis, but is defined mostly on clinical grounds. African AIDS is not
a specific clinical disease, but a battery of previously known and thus totally un-specific
diseases:(63, 104)
- loss of weight (> 10% of normal body weight), and
- chronic diarrhoea (lasting at least two months), or
- chronic fever and asthenia, plus
- persistent cough,
- generalised pruritic dermatitis,
- recurrent herpes zoster,
- candidiasis oral and pharyngeal,
- chronic or persistent herpes,
- cryptococcal meningitis,
- Kaposi’s sarcoma.
Yet these symptoms are common, non-specific manifestations of many diseases that are
endemic in Africa and have been there long before the AIDS era:
- Kaposi's Sarcoma, classified in Western countries as one of the ‘definitive
diagnoses’ or a ‘presumptive diagnosis’ for AIDS-indicator diseases, has
been present in Africa since antiquity. Its characteristic clinical features are
described in the Ebers papyrus that dates from 1600 BC.
- “Recognition of paediatric AIDS is particularly difficult in Kinshasa [Zaire],
since many children have severe infant and childhood diseases with similar
manifestations (e.g. weight loss, chronic diarrhoea).”(64)
58
- ‘Slim disease’ is a wasting syndrome seen in Africa since the first
colonisation, and although it would not fall under any categorisation of AIDS
by the standard empirical definition, it is nevertheless being considered as
AIDS in Africa.

Immune deficiency in Africa

- “Tuberculosis, protein calorie malnutrition, and various parasitic diseases can
all be associated with depression of cellular immunity.”(59)
- “A wide range of prevalent [in Africa] protozoal and helminthic infections
have been reported to induce immune deficiency.”(60)
- “Among healthy Africans resident in an area with no AIDS diseases, the
number of helper [T4] and suppresser [T8] lymphocytes were the same in
HTLV-III/LAV [HIV] seropositive and seronegative subjects.”(61)
- “Africans are frequently exposed, due to hygienic conditions and other
factors, to a wide variety of viruses, including the Cytomegalovirus (CMV),
Epstein-Barr virus (EBV), and Herpes Simplex Virus (HSV), all of which are
known to modulate the immune system. Furthermore, the Africans in the
present study are at an additional risk for immunological alterations since
they are frequently afflicted by a wide variety of diseases such as malaria,
trypanosomiasis, and filariasis, that are also known to have a major effect on
the immune system.”(62)

Antibody test for HIV in Africa

The data presented by the WHO and UNAIDS announcing in 1998 that Africa had
gained 23 million living with HIV/AIDS refers not to people who have developed AIDS
diseases, but to people who are considered, largely by projected estimates, to be HIVpositive.
The figure is not the result of 23 million individual positive tests.(105)
Moreover, the fact that the HIV test is a non-specific antibody reaction has become
more obvious than ever in African patients tested for AIDS. The cross-reactivity to
antigens presented endemically in the blood of African people is forcing scientists to reevaluate
the specificity of the test. At the same time it produces very false statistics on
the true extension of the ‘AIDS epidemic’ in the African continent.
59
“Leprosy patients and their contacts show unexpectedly high rates of falsepositive
reactivity to HIV-1 proteins on both Western Blot and ELISA.” The
cross-reactivity was found to be caused by antibodies directed against two
major carbohydrate-containing M. leprae antigens, phenolic glycolipid-I and,
in particular, lipoarabinomannan (an arabinose-containing lipopolysacharide)
which is also present in M. tuberculosis and other mycobacterium. So
“ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic
areas of Central Africa where the prevalence of mycobacterial diseases is
quite high.”(65)
The cause of tuberculosis is a mycobacterium. Tuberculosis has been endemic in Africa
for generations. Of the 661 million people living in sub-Saharan Africa, 2-3 million have
active TB with an annual mortality of 790,000. Since the AIDS era, tuberculosis has
become one of the AIDS-indicator diseases, indeed 30-50% of African ‘AIDS deaths’
are from TB. A 1986 study in a tuberculosis sanatorium in Kinshasa (Zaire) shows that
half of the suspected pulmonary cases, one third of the confirmed cases and two thirds of
the confirmed extra-pulmonary cases had a positive Western Blot antibody test.(67)
Having seen the capacity of cross-reaction between ‘HIV proteins’ and mycobacteria,(65)
what the test is showing is precisely a non-specific antibody reaction that indicates an
abnormal immunilogical state in TB patients.
The annual mortality rate in the sub-Saharan region is 12,300,000 deaths, 75,000 of
which are considered to be HIV-related. Between 30 and 50% of the HIV deaths are
from TB, but every year, as I have said, another 790,000 people die from TB in the same
region.
During the African AIDS epidemic the sub-Saharan population has grown at an annual
rate of about 2-6% per year—from 378 million in 1980 to 652 million in 2000 (U.S.
Bureau of the Census International Data Base 2001). Thus Africa had gained 274 million
people since 1980. According to the report of the WHO (World Health Organisation
2001b), during the same period of time, the African AIDS epidemic has produced a
cumulative total of 1,093,522 deaths. Therefore a theoretical above-normal loss, due to
AIDS, of one million Africans over a period in which over 200 million were gained is
statistically hard, if not impossible, to verify, unless again the African AIDS diseases
were highly distinctive. But the list of African AIDS diseases cannot be clinically
distinguished from their conventional counterparts, only the test can make the
distinction, while the WHO decided in Bangui, Africa, in 1985 (the Bangui definition of
African AIDS), to accept African AIDS diagnoses without the HIV-Test. This was done
because these tests were unaffordable to most African countries (WHO, 1986).
60
The question then arises whether the mortality claimed for AIDS (0.6% of the annual
death rate) is in fact new mortality that can be distinguished from conventional mortality,
or whether it is a minor fraction of conventional mortality under a new name. The
conclusion is that both acquired immune deficiency and the symptoms and diseases which
constitute the clinical syndrome are long-standing in Africa.
Indeed, all the available data is compatible with an old African epidemic, that of
malnutrition and poverty-associated diseases. Only the name is new.
However, the naming of the disease is crucial because it defines the treatment.
If we look again at epidemiological data on the HIV ‘estimates’ we come to another
astonishing revelation. In Africa the 23 million estimated pool of HIV-positives (carriers)
generate, as seen before, 75,000 cases of AIDS per year, which means one AIDS case
per 300 HIV-positives. But in the USA, the pool of 900,000 HIV-positives generates
45,000 AIDS cases per year (Centres for Disease Control, 1999), which means one
AIDS case per 20 HIV-positives. Thus the risk of developing AIDS for an American
HIV-positive is about 15 times higher than for an African. Now, since over 150,000
healthy (!) HIV-positive Americans are currently treated with DNA chain-terminators
and other anti-retroviral drugs,(113) as a measure to pre-empt or delay the development of
AIDS, but since the American HIV-positives develop 15 times more cases of AIDS than
their African untreated counterparts, to look at the AIDS treatments now becomes
imperative.

G) ANTI-RETROVIRAL DRUGS: THE TREATMENT FOR HIV-AIDS

The therapeutic agents for AIDS are another astonishing aspect of this phenomenon. All
the AIDS drugs in the market are extremely toxic and work by producing immune
suppression. The use of immune-suppressive drugs against an immune-deficient patient is
an enormous therapeutic contradiction.
The rationale behind it is purely theoretical. So far, in 2004, it is still an assumption based
on in vitro models, that the virus produces immune deficiency by killing T4 lymphocytes.
The correlation of T4-cell depletion in AIDS patients is not enough to assume that the
loss of T4-cells is due to the action of the virus. An even greater assumption is that by
killing the supposed virus, the depletion of T4-cells will stop and health will be restored.
Cancer research is in fact the arena of this phenomenon. The therapeutic arsenal for
cancerous malignancies of white cells (leukaemias) are drugs designed to block the
excessive cellular proliferations that these malignancies produce. Their chemical action is
61
directed at stopping these fast-growing numbers of cells by toxically suppressing the
bone marrow. These chemotherapeutics are highly poisonous drugs. They are very
sophisticated immune suppressants that, by their toxic and suppressive effect, reproduce
a toxicological immune deficiency, parallel to the one that the patient already has. Anti-
HIV drugs cause AIDS-defining and other specific diseases, regardless of the presence of
antibodies to HIV.
The fundamental problem of any chemical anti-virus ‘therapy’ is that the cell carries out
all viral biochemical functions. Thus all anti-viral treatments are inevitably anti-cell
treatments. All of the anti-retroviral drugs come from cancer research:

Azidothymidine (AZT)

AZT has been the first drug marketed for the treatment of HIV-AIDS. But AZT was
developed in 1964, twenty years before the discovery of HIV. Jerome Horwitz of the
Detroit Cancer Foundation, financed by the NIH, created a chemically modified form of
a DNA building block. When a cell is about to divide it makes a copy of its genetic
material by growing a new chain of DNA. Horwitz’s altered DNA building block enters
that new chain, blocking further DNA growth by stopping further DNA blocks from
being added. The cell cannot copy its DNA sequence and dies trying. AZT was a perfect
killer of dividing cells.
Experiments conducted on mice with cancer showed no result of stopping cancer, but an
extreme toxicity that resulted in the death of the mice. The drug was shelved. But later
the anticipation paid off.
After the 1984 announcement of HIV as the cause of AIDS there was a real rush to find
a therapeutic agent against the virus. Many pharmaceutical companies joined the race.
David Barry, the head researcher at the U.S. branch of Burroughs Wellcome, selected a
handful of previous rejected substances, among them AZT, and sent them to Wellcome’s
former collaborators. If one of these could be approved, the company would save vast
sums of money on research and development. The political pressure of the time for a
quick solution played in his favour.
Winning the approval of a drug by the FDA (American Food and Drug Administration)
implies that the agency bans most potential drugs, automatically suppressing the
competition and granting treatment monopolies for approved drugs. This monopoly
alone can be worth hundreds of millions of dollars to the pharmaceutical company
holding the patent.
62
D. Bolignesi, a veteran retrovirus researcher, found that AZT was the most potent
compound in stopping the multiplication of cells infected with HIV in the test tube. Barry
contacted Sam Broder, in charge of Gallo’s laboratory at the National Cancer Institute.
The three of them subsequently published the scientific paper.(114) The therapeutic dose
of AZT able to destroy the virus was, according to the paper, 1000 times smaller than
the one that could kill the T-cells, where the virus allegedly is. This theoretically meant
that small doses of the drug could stop HIV without seriously damaging the immune
system of the patients. The compound was classified as a reverse transcriptase
terminator.
However, AZT does not attack reverse transcriptase directly. It only stops DNA
synthesis, as it was designed to do in the first place. Since retroviruses can make viral
DNA only in cells making their own DNA, and the T-cell has to copy one hundred times
more DNA than the small virus, AZT is 100,000 times more likely to block cell DNA
and kill the cell than to block the viral DNA. Moreover, like any other chemotherapeutic
drug, AZT is unable to distinguish between an HIV-infected T-cell and the other noninfected
T-cells, and since only 1 in 500 T-cells is ever infected even in patients dying
from AIDS,(108) AZT needs to kill 499 good cells for every cell that is infected. This is
not a good therapeutic index.
Nevertheless, AZT was rushed through Phase I trials, the tests that determine toxicity for
humans. The Phase II study is to see whether the drug could stop the development of
AIDS.
Double-blind placebo-controlled studies are the cornerstone of Phase II. This rigorous
gold standard is the fundamental control for any promising drug. A study was published
in 1987.(115) Burroughs Wellcome not only co-authored the study (Drucker, Nusinoff-
Lehrman, Segreti, Rogers, Barry) but also paid for the licensing study of what was
already its own product. The study had to be aborted early for a variety of reasons. But it
concluded that AZT had a good response with a quick increase in the depleted T4-cells.
The short duration of the trial (less than 4 months) did not allow anyone to see that the
apparent increase of T4-cells was not a curative action of AZT, but only a homeostatic
temporary reaction by which the body was increasing the production of T4-cells that
were being depleted by AZT. The increase would later wear off as the progressive
depletion caused by the toxicity of AZT eventually overcame the body’s self-repairing
capacity.
But what the study did already show were signs of high toxicity developing in patients
that took the drug in comparison with the placebo group. These were somehow largely
overlooked. The rumour of an effective drug against AIDS being on trial spread like
63
wild-fire among the increasingly terrified population of HIV-positive homosexuals.
David Barry demanded special permission from the FDA for Burroughs Wellcome to sell
AZT while waiting for the official approval, so the FDA granted permission to use an
Investigational New Drug (IND). In February 1987 the FDA finally approved AZT.
Burroughs Wellcome quickly patented the drug.
The medical manufacturer Burroughs Wellcome sold the drug under the commercial
name of RETROVIR (AZT), in the form of capsules of 100mg each. The manufacturer
does not warn about the toxic effects of AZT.
The biochemical manufacturer Sigma Chemical Co., on the other hand, marketed the
drug under the commercial name ZIDOVUDINE (AZT). Their 100mg capsules come in
a bottle with a label that has the skull-and-crossbones symbol for unusual chemical
hazards. The warning reads: “TOXIC. Toxic by inhalation, in contact with skin and if
swallowed. Target organ(s): Blood bone marrow. If you feel unwell, seek medical advice
(show the label where possible). Wear suitable clothing.”
The daily recommended dose at the time was 500mg for asymptomatic HIV-positives,
and 100mg prescribed to pregnant, HIV-positive mothers.
The toxicity of AZT is due to its targeting of bone marrow. AZT does what it was
designed for, to destroy DNA replication, and with it the cell. AZT is cytotoxic. It
suppresses the bone marrow, depleting the organism of the same T-cells that HIV is
supposed to attack, so it is immunotoxic. The immune-suppressive action of AZT ends
up by producing an acquired immune deficiency. Asymptomatic HIV-positive patients
taking the prescribed doses of AZT develop:(106)
- Lymphoma (in 46% of patients after 36 months of treatment)
- Dementia
- Weight loss
- Yeast infections
- Pneumocystis pneumonia
The problem is that all of the above diseases are AIDS indicator diseases. So the
progressive deterioration of health and the eventual death are seen as the unfortunate
development of AIDS in previously asymptomatic HIV-positive men. The cruel truth is
that the chemical compound that they are taking is replicating the supposed mechanism
of action of HIV: it destroys T-cells, but at a faster rate.
Considering their mechanism of action, all the DNA chain-terminators are inevitably
cytotoxic and immunotoxic, like most other chemotherapies.
64

DDI: another DNA chain-terminator produced by Bristol Myers Squibb

This new drug with a similar action to AZT added two more toxic effects not observed
with AZT: fatal pancreatic damage and neural peripheral destruction (Merck Index).

HIV protease inhibitors

The HIV protease inhibitors were designed to inhibit specifically auto-proteolytic
processing of HIV proteins, which is necessary for HIV assembly.
The doses at which these inhibitors ‘block HIV replication’ in the test tube (we must not
forget that the proof of blocking is indirect, by looking for RT), did not produce any
evident therapeutic effects.
The doses were increased to 4-5 orders of magnitude above what is needed to render
HIV non-infectious in vitro, or to 1-2 grams per day.(115)
Saquinavir by Roche and Ritonivar by Abbot are two of these new retrovirals. The
toxicity of these drugs is enhanced by the amounts prescribed. The doses currently
administered to patients are at least 50 times higher that what is needed to completely
inhibit the cellular intestinal aspartyl protease cathepsin D. The destruction of cathepsin
D accounts for anorexia (weight loss) and diarrhoea. Affecting probably, as it does in
mice, the thymus and spleen, a massive loss of T-cells and B-cells leads to death.
We see the same pattern that we saw with DNA chain-terminators. The toxic effects of
the protease inhibitors can cause at least three AIDS defining diseases.

Drug cocktails

AZT and other DNA chain-terminators are now typically supplemented by inhibitors of
proteases to form drug ‘cocktails’. A daily dose of these includes about 1g of one or
more DNA chain-terminators per clinically ill person, and 0.5 g per asymptomatic HIVpositive
per day, which is equivalent of 1.5 to 3 x 106 molecules of DNA chainterminator
per body cell.
65

Nevirapine

Nevirapine is an anti-retroviral drug manufactured by Boehringer Ingelheim/Roxane and
commercialised under the name of Viramune. Nevirapine is one of the anti-retroviral
drugs that has been promoted for stopping mother-to-child transmission of HIV.
Especially in Africa, Nevirapine has been pushed hard for use in pregnant women. That
use of Nevirapine comes from a single study, the 1999 Uganda study. In the study, “a
single 200mg tablet was given to the mother at the onset of labour, and a single dose of
nevirapine suspension 2mg/kg for the neonate administered at 72 hours after birth or at
discharge from hospital, whichever occurred first.”(143)
The study claims to have reduced the percentage of HIV transmission (15-30%) further
than AZT, and it campaigns for the use of Nevirapine instead. But since Nevirapine, like
AZT, due to its pharmacological mode of action, is capable only of preventing infection
of cells not already infected and is unable to inhibit the expression of HIV within already
infected cells or eradicate the virus, when the drug is given to neonates, especially 3 days
post partum, it will have no effect on mother-to-child transmission in utero or during
labour and delivery. Nor will the single dose of 200mg of Nevirapine have any effect on
the mother’s milk, because it does not reach the concentration necessary to have an antiretroviral
effect. The same happens with the single dose given to the infant.
The European Agency for the Evaluation of Medicinal Products (2000) recommends the
use of Nevirapine only for combination therapy and only for “infected patients with
advanced or progressive immunodeficiency.”
Nevirapine monotherapy does not have a significant effect on the increase of T4-cells
and does not inhibit progression to AIDS.(144, 145)
The following information is quoted from the Physicians Desk Reference (PDR), 2001
edition:(38)
- Nevirapine is a non-nucleoside reverse transcriptase inhibitor that belongs to
the dipyridodiazepinone chemical class of compounds.
- Nevirapine binds directly to reverse transcriptase and blocks the RNAdependent
and DNA-dependent DNA polymerase activities by causing
disruption of the enzyme’s catalytic site.
- Animal studies have shown that nevirapine is widely distributed to nearly all
tissues and readily crosses the blood-brain barrier. It is also widely
distributed in humans, readily crosses the placenta, and is found in breast
milk.
66
- Nevirapine is known to be active in peripheral blood mononuclear cells,
monocyte derived macrophages, and lymphoblastoid cell lines.
- Nevirapine is known to increment oxidative metabolism in humans. In vivo
studies in humans and in vitro studies with human liver microsomes have
shown that nevirapine is extensively biotransformed via cytocrome P450
metabolism to several hydroxylated metabolites. Nevirapine is extensively
metabolised by the liver and nevirapine metabolites are extensively eliminated
by the kidneys. However, the pharmacokinetics of nevirapine have not been
evaluated with either hepatic or renal dysfunction.
- The relationship between in vitro susceptibility of HIV-1 to Nevirapine and
the inhibition of HIV-1 replication in humans has not been established. At the
present, there are no results from controlled clinical trials evaluating the
effect of Viramune (nevirapine) in combination with other anti-retroviral
agents on the clinical progression of HIV-1 infection, such as the incidence
of opportunistic infections or survival.
- Patients should be informed that Viramune therapy has not been shown to
reduce the risk of transmission of HIV-1 to others through sexual contact or
blood contamination.

Side Effects

The long-term effects of Nevirapine are unknown at this time [year 2001].
There are no adequate and well-controlled studies in pregnant women.
Nevirapine should be used during pregnancy only if the potential benefit
justifies the potential risk to the foetus.
Nevirapine produces significant decrease in foetal body weight. The
evaluation of the pharmacokinetics of nevirapine in neonates is ongoing and
the safety profile in neonates has not been established. Three clinical trials
with nevirapine in paediatric patients reported an overall incidence of related
adverse events in 46% of children.
Nevirapine causes anaemia, thrombocytopenia and granulocytopenia,
especially in paediatric patients.
67
WARNINGS: Severe life-threatening skin reactions, including fatal cases,
have occurred in patients treated with Viramune. These have included cases
of Steven-Johnson Syndrome, Toxic Epidermal Necrolysis, and
hypersensitivity reactions characterised by rash, constitutional findings and
organ dysfunction. Patients developing signs or symptoms of severe skin
reactions or hypersensitivity reactions must discontinue Viramune as soon
as possible.
Severe and life-threatening hepatotoxicity, including fatal Hepatic Necrosis,
has occurred in patients treated with Viramune.
Resistant virus emerges rapidly and uniformly when Viramune is
administered as monotherapy, therefore, Viramune should always be
administered in combination with anti-retroviral agents.
There is a more sinister aspect to these drugs besides their toxicity. By producing
immune-suppression, they are toxically inducing an immune deficiency that replicates the
one from which the patient is already suffering. What the anti-retroviral drugs in fact do
is to further increase the immune deficiency by selectively destroying T4-cells, and the
patient ends up dying and fulfilling at the same time the expectation that the virus is
cytophatic for T4-cells, and kills the patient by depleting the immune system of these T4-
cells. The drugs do this even more effectively and quickly than the virus. The virus can
take up to 20 years to develop into AIDS. With sustained treatment using anti-retroviral
drugs, you can be dead in 3 or 4 years.
68

V. DECONSTRUCTION OF THE APPARENT PARADOX

Initially we have looked at the epidemiological data on AIDS and encountered
paradoxical behaviour in the epidemic. Furthermore, we have realised that the paradox
was in fact created artificially by judging the cause of the epidemic to be a single
infectious agent, the retrovirus HIV.
More doubts arose while looking at the above evidence on HIV. These doubts can be
summarised as follows:

Reasons to doubt that HIV is the cause of AIDS

a) Because of its non-randomness

The most striking characteristic of the U.S. and European epidemic has been, and still is,
the specific distribution of AIDS—what we called at the beginning the geography of
AIDS.
AIDS in the USA and Europe continues to affect the same group of people: male
homosexuals (2/3), intravenous drug-users (1/3), 1% are haemophiliacs and other
transfusion recipients, and 1% are children born to drug-addicted mothers.
A recent report from the WHO (September 2003, HIV/AIDS in the European Region)
confirms the same pattern:
“The European Region is experiencing the fastest growing HIV epidemic in
the world, and significant further growth is likely. Between 1995 and 2003,
the number of newly reported HIV-positives in western Europe doubled to
almost 170,000, and in central and eastern Europe grew from 27,000 to
320,000. It is now estimated that at least 1.7 million people in Europe are
already HIV-positive.
An epidemic of injecting drug use is fuelling the HIV epidemic. In the former
Soviet Union, where 2/3 of all Europeans infected with HIV live, 84% of all
HIV cases with a known transmission route are attributed to injecting drug
use.
In western Europe sexual transmission is the dominant route, with the largest
number of infections among men who have sex with men.”
69

b) Because other factors present in all of the AIDS cases can account for the same
AIDS-specific diseases, with the same hallmark of T-cell depletion.

The homosexual group
The major sources of Acquired Immune Deficiency in this group are immune suppression
caused by:
I. Toxicity of prescription drugs
Ia. Anti-retroviral drugs
About 2/3 of all AIDS cases (deaths) in the USA and Europe are among male
homosexuals. Of the group of AIDS-specific diseases, this group typically develops
Kaposi’s sarcoma, lymphoma, dementia, weight loss, yeast infections and pneumocystis
pneumonia.
Apart from Kaposi’s sarcoma, these diseases are developed by all patients under longterm
prescription of AZT. The immune suppressive effect of the retroviral chemotherapy
efficiently kills the patient in the same way that the virus is supposed to. Since about
450,000 U.S. citizens are currently on DNA chain-terminator and protease inhibitors as a
prophylaxis against or a therapy for AIDS, these drugs alone could have been sufficient
to cause all of the 43,158 AIDS deaths reported in the USA in 2001.
Ib. Other prescription drugs
Gonorrhoea, syphilis, hepatitis B, herpes and amoebiasis are much more common in
homosexual males than among heterosexuals. Also, homosexual males develop various
bowel infections that cause persistent and recurrent diarrhoea.(121) Most of the agents
used for the treatment of these diseases are oxidising, mitogenic and immune-suppressive
agents.(122)
Steroids and antibiotics are probably among the most abused medical substances in this
group.
70
Ic. Other viruses in homosexuals
Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are present among homosexual
men as well as in the rest of AIDS patients. Both viruses produce clinical and
immunological abnormalities similar to those seen in AIDS patients. These viruses induce
immune suppression in vitro and in vivo, including abnormalities in the T4/T8 ratio both
in humans and animals. Both viruses have been isolated from many sites, including KS,
from almost all AIDS patients.(121) Unlike the above viruses, HIV has never been isolated
in fresh AIDS tissues.(123)
II. Toxicity of recreational drugs
Kaposi’s Sarcoma only develops among male homosexuals using Nitrite inhalants. These
drugs are immune-suppressive, mitogenic, and carcinogenic.(120)
Studies post-1984 show categorically that male homosexuals with AIDS or at risk from
AIDS have continued to use nitrite inhalants, amphetamines, cocaine, heroin, and
steroids.
III. Immune-suppression by anal sex
“Receptive anal intercourse accounted for nearly all new HIV infections among
homosexual men enrolled in this study.” (Multicenter AIDS Cohort Study of 4995 male
homosexuals).(119) What that means is that the rectal absorption of sperm was responsible
for the immune-suppression. Sperm is a strong immune-suppressive agent. Mature sperm
is much more effective in producing immune-suppression than immature sperm. Mature
sperm is a highly oxidising agent. Oxidation of the host immune system leads to immunesuppression.
The critical structural difference between the epithelium of the rectum and vagina reveals
how biologically unnatural anal intercourse is. The vagina is lined with a thick stratified
squamous epithelium that makes ulceration and penetration of the semen into the
vascular lamina unlikely. In contrast, the semen in the rectum is separated from blood
vessels and lymphatics by a single layer of cells that is easily penetrated and ulcerated
during anal intercourse. “In addition to lymphoma and Kaposi’s sarcoma, the male
homosexuals develop another two malignancies: cancer of the tongue and rectum.”(121)
71
The Intravenous drug-user group
About 1/3 of all AIDS cases in the USA and Europe are male and female intravenous
drug-users, and of those, 75% are male.
The AIDS-defining diseases that this group commonly share are: tuberculosis++,
dementia+, weight loss+, yeast infections+, pneumocystis pneumonia+.
Heroine, cocaine and amphetamines are oxidising agents, just like amyl nitrite.
Immunological and clinical abnormalities similar to those seen in AIDS have been
reported in drug abusers as far back as 1973.
- Immunological abnormalities include: absolute lymphopenia (low count of
lymphocytes), decreased concentration of IgM and IgG antibodies, and falsepositive
results to many serological tests in as many as 40% of intravenous
drug-users.
- Clinical abnormalities include: lymphadenopathy ranging from benign
hyperplasia to malignant lymphoma, other malignancies, fever, night sweats,
chills, weight loss and increased susceptibility to opportunistic infections.
Transfusion recipients group
1% are haemophiliacs and other transfusion recipients.
“The abnormal T-lymphocyte subset is a result of the intravenous infusion of Factor VIII
concentrates per se, not HTLV-III (HIV) infection.”(118)
Factor VIII has been found to be immune-suppressive both in vitro and in vivo, the
T4/T8 ratio being inversely correlated with the quantity of factor VIII concentrate
administered. Factor VIII is a high molecular weight glycoprotein complex, whose
subunits are linked by a large number of SS bonds. The oxidant activity comes from the
SS bonds needed for agglutination activity. Evidence exists that all clotting agents are
oxidising agents. Randomly selected patients from the haemophiliac group and from the
male homosexual group show that 70% of the haemophilic group was reported to be
HIV-positive compared to 45% in the homosexual group, but only 0.06% of
haemophiliacs develop AIDS.(124) As in all other AIDS patients, the virus in these groups
has been isolated only in vitro.(125)
72
The artificially sustained life of the T-cell in a test tube has revealed the proteins used for
the test. This means that the HIV test, at best, is an indirect test that correlates immunesuppression
with the appearance of certain proteins.
Children group
1% are children born to drug-addicted mothers.
Most babies with AIDS in the USA and Europe are born to mothers who have used
recreational drugs (heroine, cocaine, amphetamines) intravenously during pregnancy, but
have also used anti-viral drugs.
All HIV-positive, pregnant mothers are now treated with AZT during the last 6 months
of their pregnancy to reduce the possibility of mother-to-child transmission of HIV,
which stands at 25 to 50%. Therefore, the HIV-free babies born to these mothers—that
is, more than 50% of them—have all been treated with AZT.(126) Yet because of the toxic
effects of AZT, these HIV-free babies suffer from diseases such as fever, pneumonia,
anaemia and mitochondrial dysfunction.
There is no mother-to-child transmission of the disease. What the mother passes on to
the child is polluted blood, an immune-deficient state produced by immune-suppressive
drugs, recreational and medical.

c) Because of the difference in the epidemic’s features between countries with very
different economies

The geography of AIDS, we have seen, is even more specific. There is an AIDS of
Western developed countries—countries with thriving capitalist economies and decadent
behaviour patterns stemming from social collapse—and there is an AIDS of poor
underdeveloped countries, with endemic low protein-calorie intake, poor water resources
and sanitation, and endemic intestinal parasitosis. And in these poor countries AIDS, like
hunger, attacks at random: 50% men, 50% women.
Scientists have allocated a different virus to each type of AIDS geography, HIV-1 for the
rich and HIV-2 for the poor.
The prevalent U.S.-European AIDS-specific diseases:
73
Pneumocystis pneumonia ++ (homosexuals and iv-drug-users)
Kaposi’s sarcoma ++ (homosexuals—nitrite inhalants)
Lymphoma + (AZT)
Weight loss + (AZT, retrovirals, iv-drugs)
Yeast infections + (AZT, retrovirals, antibiotic overuse, iv-drugs)
Dementia + (AZT)
Tuberculosis ++ (characteristic of iv-drug-users)
Bacterial pneumonia ++ (children in USA and Europe)
The prevalent African AIDS-specific diseases:
Tuberculosis ++ (endemic: almost 3 million per year in sub-
Saharan region)
Weight Loss ++ (slim diseases; endemic under-nourisment)
Bacterial pneumonia + (children and adults antibiotic resistant)
Diarrhoea + (endemic intestinal parasitosis)
If we put together both epidemics, USA-Europe and Africa, the promoting factors we
identify for the development of AIDS-defining diseases are: homosexuality, iv-drug use,
retroviral medications and other chemical pathogens, and malnutrition. Distinct chemical
pathogens cause distinct AIDS-defining diseases. Since chemicals are not self-replicating
like viruses, pathogenicity is dose- and time-dependent (i.e. it takes 20 or more years of
smoking to develop lung cancer). And since there is no immunity against drugs or
malnutrition, nor against drug- or malnutrition-induced diseases, the corresponding
epidemics are not self-limiting, as an infectious epidemic would be once natural immunity
has developed (that being the rationale behind vaccinations).
Therefore people who are not subject to drugs or malnutrition, or who discontinue drug
use or malnutrition, before irreversible damage has occurred, do not develop AIDS,
regardless of having antibodies to HIV.
What we can see is that the Acquisition of the Immune Deficiency Syndrome in the USA
and Europe is done willingly. The immune-suppression is self-inflicted by unhealthy
behaviour, or inflicted by medical prescriptions, or medical products. It is nothing other
than blood pollution, the disease of plenty.
The Acquisition of the Immune Deficiency Syndrome in Africa, on the other hand, is
done unwillingly. The immune deficiency is determined by factors beyond the control of
the sufferers. The new forms of economic colonialism are keeping the sub-Saharan
74
region under deprived poverty. It is nothing other than undernourished blood, the disease
of the poor.

Doubts regarding the cytopathic action of HIV and its route of transmission

The inference that the low count of T4 lymphocytes is the result of the cytophatic action
of HIV is based on the belief that HIV is inside the cell that is killed. The proof of the
pathological effect of HIV is based on evidence from in vitro models and epidemiological
data of the concomitance of low counts of T4-cells in patients suffering from AIDSdefining
diseases.
The heterosexual transmission of AIDS is, again, epidemiological data under the wrong
heading. Heterosexual AIDS patients in the USA and Europe are either intravenous
drug-users or haemophiliacs.
The African positive HIV-test is very important to the West. Indeed, the randomness of
Africa’s epidemic is the very proof needed to support the theory that AIDS is
heterosexually transmitted, which supports the hypothesis of a sexually transmitted
disease. Quite apart from the imperative suggestion that Africans must be very
promiscuous in order to develop an epidemic of such proportions, this is also a smoke
screen to vindicate the unnatural practice of homosexuality. The fact is that the outcome
of homosexual promiscuity is an immune deficiency, and therefore an extraordinary
unveiling of the sickness of the practice. It is contra-natura: it makes you ill. But by
blaming a virus, everyone is made to seem at risk.

Doubts regarding the diagnosis of AIDS by a positive HIV test

The test is the only common ground between these two otherwise completely different
phenomena. The core support for the HIV hypothesis is that people with AIDS have a
positive antibody reaction to the proteins of HIV. The fact that many people with AIDS
test positive shows per se a correlation but not a causation.
As explained before, the 1984 identification of HIV is scientifically unreliable, and there
is no scientific evidence that can substantiate the claim that the proteins obtained from
that experiment are viral proteins.
Strictly speaking, according to the evidence, what we have is proteins (p24 and p41),
which we know to have come from diseased lymphocytes, to which people with acquired
75
immune deficiency (low T-cell counts and AIDS-defining diseases) and people with no
immune deficiency (normal T-cell counts and good health) react positively.
This means that in both groups their blood has the ability to recognise these proteins by
means of antibodies. Having antibodies against these proteins gives no indication of,
indeed bears no relation to the state of health of the person.
Because the testing for antibodies against these proteins was never done before 1984, we
do not even know since when the human organism has had the capacity for immune
recognition of them. Furthermore, if these proteins belong to ill lymphocytes it means
that, if they are new, what they express is a phenotypic change that the disease is causing
in the lymphocytes. The proteins that trigger the antibody reaction are normal cellular
proteins, cellular proteins with new antigenic epitopes, or newly induced cellular
proteins. The immune system’s ability to spot a new protein on the surface of an ill
lymphocyte is precisely one of its inherent capacities. As we have seen in the evidence so
far, activated lymphocytes will express new molecules on their cell surfaces. The
recognition of these new molecules in somebody’s immune system only indicates that
that person has a sensitive marker for activated lymphocytes. These antibody markers
may even be hereditarily transmitted in the same way that we inherit other
immunoglobulins or endogenous retroviruses. No-one has systematically tested parents
or grandparents of adult HIV-positive patients.
“The cancer protocol of immune-vigilance (checking for specific proteins as
specific indicators of cancerous diseases) is based on a clear concept that
tumour cells express antigens that are not present in their normal
homologous tissues. The malign transformation can be accompanied by
cellular phenotype transformation, with the loss of normal antigenic
components of the cell surface and the acquisition of neo-antigens. Some of
these neo-antigens are capable of evoking an adaptive immune response.”(117)
The 1983/84 HIV test is at best a non-specific indicator of altered lymphocytic
homeostasis. The proteins represent no more evidence than that.
The test is the export from the West to Africa. With it comes the renaming of wellknown,
long-established diseases, and its unique medical value is that it defines the
treatment.
76

VI. THE LONG-RUN ECONOMIC COST OF AIDS-BUDGETS

In an article in TIME Magazine, 23 April 2001/Vol. 157, No. 16, a plan that “could save
the lives of 5 million people” was budgeted as follows:
HIV tests for 10 million people $43 million/year
AIDS drugs for 1 million patients $650 million/year
Supervision of therapy $200 million/year
Clinical treatment $230 million/year
Research costs $25 million/year
Total initial funding required $1.15 billion/year
If we take the annual GDP of the African countries, and then calculate, using the figures
given by the WHO of HIV-carriers in Africa, what the cost per country of ‘saving’ its
infected people would be, then we realise the kind of predicament the African continent
is facing.
77

VII. CONCLUSIONS

Now that we have looked at the evidence, we can start to draw conclusions.
We will begin by looking at what the Acquired Immune Deficiency Syndrome epidemic
is not:
- AIDS is not an infectious disease, is not contagious and is not transmitted
sexually or otherwise.
- AIDS is not caused by HIV—neither in the USA and Europe, nor in Africa.
Therefore, in order to be precise, we can no longer call the phenomenon HIV-AIDS.

- AIDS, Acquired Immune Deficiency Syndrome, is not a syndrome in every place in the world. In accordance with the proper meaning of the term, we have to say that AIDS only exists in the USA and Europe, and that is because:

- Acquired: only in the USA and Europe is the immune deficiency acquired—added to which, the acquisition is voluntary.

- Immune Deficiency: only in the USA and Europe is the immune deficiency produced by immune suppression. This immune suppression is self-induced by unnatural sexual practices, prescription and recreational drug abuse, intravenous toxic mania. Or it is medically induced by the prescription of anti-retroviral chemotherapy. So as we said before, it is a voluntary acquisition of immune deficiency.

- Syndrome: only in the USA and Europe can we accept that the Acquired Immune Deficiency is a Syndrome, in the sense that immune suppression is the common cause of the different AIDSdefining diseases, and therefore all these diseases can be classified as part of the same syndrome.

- Epidemic: after 1981 the AIDS epidemics of the USA and
Europe increased steadily for a decade and, after reaching peaks
in the 1990s, they decreased to about what is currently half of
their peak levels (WHO, 2001b). The new Eastern Europe
epidemic is an intravenous-drug abuse epidemic, and the
‘counting’ (HIV testing) only begun recently. The figures that make the syndrome look like an epidemic are not the numbers of people dying of AIDS, but the recorded figures of people who have tested HIV-positive. The only epidemic, if there is one, is
the one created by the test: the epidemic of tested HIV-positives together with the estimates.

- AIDS in Africa, according to the proper meaning of the term, does not exist
at all, and that is because:

- Acquired: the African immune deficiency is not acquired, but
developed by endemic poor protein-calorie intake. There is no
voluntary acquisition, rather it is imposed.

- Immune Deficiency: in Africa the immune deficiency is not
produced by the use of immune-suppressants, but is the
consequence of underdeveloped immunity, caused by endemic
malnutrition. Therefore, as we have said, it is not acquired but
developed, not voluntary but imposed.

- Syndrome: the African AIDS-defining diseases do not have
immune deficiency as their sole common cause, therefore they
cannot be associated in the same group to form a syndrome. The
different diseases of African AIDS have been endemic to the
region for a very long time and each one has its own well-known,
varying causes. In some cases immune deficiency is the cause, in
some cases it is concomitant with the cause, in some cases it is
the result of the cause, and in other cases it is not there at all.

- Epidemic: in Africa, AIDS is not epidemic but endemic: and has
always been here. The only epidemic is the epidemic of HIVpositive
estimates, by the statisticians working for the World
Bank, IMF, WHO, CDC, and other organisations. After applying
their algorithmic projections to the ‘estimated’ numbers of HIVpositive
people, or ‘carriers’ as they prefer to call them, they
arrive at terrifyingly apocalyptic numbers of future generations
wiped out.

The most frightening aspect of all is that all the economic
packages of the financial institutions (IMF, WB) come together
with these statistical projections, which of course are presented
as a liability to the nation-borrower. As a collateral the nation has
79

to undertake to ‘tackle the problem’ by giving to every AIDS
patient the expensive anti-retroviral drugs. These institutions are
on hand to lend these sums, perhaps even at a discount for
charitable reasons. But by giving the toxic anti-retrovirals to
everyone who is HIV-positive, their projections will become
true, only with one slight correction: the HIV-positive patient
will not die of AIDS, but of AIDS-treatment. Statistically it will
be the same. And aside from the loss of human life, the country
will be bankrupt in footing the bill.

After what we have said, if there is indeed any AIDS in Africa it must be from the U.S.-
European type of AIDS risk disease group, meaning: young male homosexuals, male
intravenous drug-users, young female intravenous drug-users.

Again, in order to be precise with nomenclature—the naming—we definitely would need
to have new names for the phenomenon of immune deficiency, all according again to its
geographical features. According to that the name could be:

- For the disease seen in the male homosexual group: Acquired T4
lymphopenia from immune-suppression as a result of anal sex.
- For the disease seen in the iv-drug-user group: Acquired T4 lymphopenia
from immune-suppression by iv-drug use.

- For the diseases seen in Africa: T4 lymphopenia related diseases, seen in
some cases or stages of TB, chronic diarrhoea, slim syndrome, etc.
It is also time to see what HIV is not:

- HIV is not the cause of AIDS. HIV does not produce immune deficiency.
- HIV is not a transmissible virus.

- HIV proteins, the ones that make the HIV-test, are not from a virus. The
HIV proteins come from diseased lymphocytes, stimulated and grown in a
laboratory test tube. The proteins are the phenotypic changes produced by an
ill lymphocyte. At the most, a positive antibody reaction to these proteins (a
positive HIV test) means an indirect indication of a degree of homeostatic
lymphocyte failure, most probably caused by whatever disease, past or
present, the patient providing the lymphocytes is suffering from. Therefore:
80

- The HIV test does not prove the presence of any virus.
- HIV does not exist as an individual entity. As part of a phenomenon, HIV
appears only in the confinement of the test tubes of cancer research
laboratories, where leukaemic lymphocytes are artificially being stimulated
and grown.

- HIV-AIDS is not a viral, transmissible disease that causes the immune
deficiency, which in turn causes an array of 30-odd diseases. HIV-AIDS is a
failed hypothesis, a case of bad science. In itself it is merely an artificial and
flawed correlation, and as such does not exist.

After having seen what AIDS and HIV are not, and what HIV-AIDS was supposed to
be, it is time to find out what HIV-AIDS really is.

To do this we will have to turn the whole affair upside down and look at it from a
phenomenological viewpoint. The phenomenon will appear clearly in front of us as soon
as we are able to identify where it takes place—the existential arena of the
phenomenon—and what the indicators of the phenomenon are—that by which it acquires
its meaning, the meaningful references, the references that give reality to the
phenomenon. So, let us look at the biographical aspect of HIV-AIDS, at the
chronological coming-into-being of the phenomenon, to see where it begins and where it
ends.

In so doing we will establish the conditions to allow the real phenomenon behind the
apparent HIV-AIDS to show itself to us, from itself, from its own reality, as itself, as
what it is.

- 1964. The first element to appear in the existential arena is the drug that
destroys the DNA of viruses that can supposedly cause cancer, that is the
DNA chain-terminator, AZT. This chemotherapy drug was designed for a
virus that would produce cancerous malignancies. The virus and the
cancerous diseases that the virus supposedly produces are yet to be found.
So the drug ‘needs’, as it were, a disease, a cancerous malignancy, and a
virus that causes it, to fulfil its destiny intended by the manufacturer: to be a
cancer therapeutic drug prescribed everywhere.

- The second element to come into being is the set of specific laboratory
biological tools.

81
Analytical laboratory tools are in one way or another a counting mechanism.
Counting requires that you look for something that can be counted. But
because they did not have the disease yet, nor the virus either, the specific
laboratory diagnostic parameters that would allow them to measure the
phenomena (how to diagnose the presence of the virus and the action of the
virus) were the outcome of the counting elements, the tools. In fact, the tools
ended up determining the parameters, not the other way around as should be
the case. ‘Techne’ sets the enframing, the way in which things need to be
looked at in order to be countable. All of these analytical tools produced
indirect evidences to sustain the apparent phenomenon of HIV-AIDS. These
tools were:

- 1970. Reverse transcriptase (RT). An exclusive viral-replication enzyme
from a leukaemia cell (lymphocyte) appeared. It was a particular DNA
polymerase. This enzyme was believed to be exclusive to retroviruses. So
finding reverse transcriptase became the indirect method of identifying the
presence of a retrovirus. Science now knows that RT also occurs naturally,
and is produced in especially large amounts in fast-dividing cells such as
lymphocytes in the bone-marrow. Finding RT is therefore no longer specific
proof of retroviruses.

- 1975. Interleukins 2 (IL2). Interleukins are growth factors (IL-1 and IL-2)
that allow the growth of leukocytes in a test tube. Confirming the hypothesis
of the retrovirus required the cultivation of cells for long periods in order for
the virus to reveal its proteins. The need for cellular growth in a test tube
brought about interleukin-2. In fact, R. Gallo himself was involved in the
discovery of T-cell growth factor, as he called it, which is now know as
interleukin-2.

- 1975. HT23V. The first human retrovirus, found by R. Gallo in lymphocytes
from a rare form of leukaemia. It was a mistake, and is no longer mentioned
in text books.

- 1977. HTLV-I. Now the first known leukaemia virus. Found by R. Gallo.

- 1979. HTLV-II. Second human retrovirus from another type of rare
leukaemia. Also found by R. Gallo.

- 1980. Analytical technology with monoclonal antibodies allows scientists to
count CD4+ subsets of lymphocytes for the first time. Selective immune
deficiency of T-cell lymphocyte appears in the medical arena.
82

- 1984. HTLV-III or HIV is officially declared to be the cause of AIDS.
Third human retrovirus discovered, also by R. Gallo. Now we can see why
the other two medically irrelevant retroviruses are so important. They give
reality to HIV by giving it a historical background: a family, a ‘belonging’.
HTLV-I and II are oncoviruses because they produce cancer, HTLV-III or
HIV is a lentivirus because it is slow, and all of them ‘belong’ to the family
of retroviruses. The imagination of Gallo went so far as to suggest that the
slave-trade and African monkeys were the route by which the virus might
have reached the West.(127)

- 1984. The HIV test appears. It was made from viral proteins that appeared
in a mixture of blood from different AIDS patients, grown in a clone of a
lymphocyte cell line from a patient with adult T-cell leukaemia, kept alive for
more than ten years in a test tube lab. These proteins are the antigens for the
HIV test. The HIV test is patented. The diagnostic tool is finalised. HIVAIDS
is marketed world-wide. The test spawns a new epidemic of HIVpositive
people.

- 1987. The first anti-retroviral AZT appears on the pharmaceuticals market.
R. Gallo was also indirectly involved in the trials for licensing the drug. AZT,
after 20 years of existence on a laboratory shelf, became the saving drug for
AIDS. Patented by Burroughs Wellcome, it was commercialised under the
name Retrovir. Every HIV-positive person in the USA and Europe, with or
without AIDS symptoms, was advised by the medical establishment to begin
to use it.

As we can see, the phenomenon of HIV-AIDS begins with anti-cancer drugs (AZT) and
ends up with anti-retroviral drugs (AZT and others).

A thing comes into being by the driving force that surges out of its need to fulfil its
purpose of existence, that for which the thing was created. The core of ‘techne’ unravels
creation (nature) as ‘a standing reserve’ for future profit. Profit, in our days more than
ever, defines the direction of research. Routes of investigation are pursued to the end,
only when a good profitable outcome can be foreseen. In pharmaceuticals, that means
developing a new drug that could be licensed for a disease that has no previous
successful treatment, or no treatment at all. The markets of the pharmaceutical
conglomerates are the human diseases themselves, and for the last sixty years cancer has
been at the top of the research agenda for most of the big companies. Since the 1950s,
pharmaceutical drug development has been shaped to a great degree by cancer research.
83

Cancer research has long been pursuing the idea that cancer can be transmitted by a
virus, since this can bring good profits. If an oncovirus is the cause of cancer, this
reduces the target of the treatment to a single cause. Therefore, targeting the virus means
treating cancer specifically. If the cause of cancer were your life-style, then the cure
would be to change that life-style, but that hypothesis is not that profitable, at least not
to the pharmaceuticals. A single agent that can be targeted by a sophisticated drug, on
the other hand, can be a winner.


The phenomenological approach allows us to conclude as follows:
The phenomenon in itself is the development of specific drugs for cancer treatment.
The meaningful references are the analytic laboratory tools that cancer research, in its
quest for the virus, has itself developed.

The existential arena is cancer research grants, cancer research laboratories and their
retrovirologists, looking for viruses among the pathological output of the decadent, postindustrial, capitalist American society and its European counterpart.

The goal of the phenomenon is the ultimate existential purpose of that specific drug,
which is to find the disease for which it has been developed, in order to fulfil the ultimate
purpose of its creation: the use of the drug by the sufferers of the diseases. And if it is the
only drug on the market for that disease, all the better. Since the drug has achieved its
goal in a sustained manner for the last 20 years, after reflecting deeply, we can only
conclude that what appears in the HIV-AIDS phenomenon is the unfolding of a
successful marketing scheme.

That marketing scheme is done almost exclusively by the test. The test defines the new
market: the new disease of HIV-AIDS. Phenomenologically speaking, we can say that
HIV-AIDS is only a new disease as long as HIV is attached to AIDS as a definition. HIV
has made AIDS a new disease, the disease for anti-retroviral drugs, and has lent it its
epidemic proportions of millions of HIV positives.
Hence, the HIV test is the most pivotal reference of meaning, because medically it is the
foundational parameter that confirms the disease, the treatment and the prognosis.
Without HIV, AIDS would still exist, but no anti-retroviral drug would be used for it.
Therefore HIV is there only to sustain the production and prescription of anti-retroviral
drugs. A legal drug cartel.

84
After twenty years this marketing scheme is still in place and thriving. New markets have
been opening in Africa, India, China and now, with the new Russia and the new EU
members, the market of Eastern Europe is emerging.
When a new drug is licensed by the FDA and patented, the pharmaceuticals company
practically acquires a monopoly over the market. So, ‘anti-retroviral-drug-against-HIVAIDS’ being the main phenomenon—the real phenomenon—means that the phenomenon itself is also patented.

The way to patent a medical hypothesis is by dogma. Once it acquires the status of a
dogma, the hypothesis becomes immune to any review, critique, or opposition. Nothing
can harm it, because no-one can question it. That is the only way in which a flawed
hypothesis can withstand the passage of time, which otherwise proves it wrong in its
predictions, wrong in its therapeutic approach and success, and wrong in its prophylactic
measures.

With all the available funds for research in prophylaxis, besides the ancient condom, no one has come up with a vaccine after 20 years of constant research, whereas in a matter
of months we get a flu vaccine for every new flu virus (with much greater amount of
DNA) that emerges in China. Of course, the dogma will immediately say that these
retroviruses are far more complicated, that they mutate, and so on. Any explanation will
do, since every honest scientist is working within the enframing of the hypothesis that by
definition is unquestionable.

And if anyone dares to question or shed doubt about the fundamentals of the hypothesis,
they will be cast out and their scientific findings will no longer reach the pages of those
prestigious scientific journals (Lancet, Nature, Science, etc.) which set the guidelines of
the medical trade by feeding the medical practitioners with the latest output of the
research community. Dissidents will also encounter the opposition of the in-the-frame
health professionals, whatever their field might be. Scientists like P. Duesberg,
E. Papadopulos and The Group of Perth University, Australia, along with hundreds of
other clear minds, have been progressively silenced.

The dogma cannot be questioned by anyone. Not by scientist, nor indeed by Head of
State.

When President Thabo Mbeki of the Republic of South Africa had the courageous will to
say no to anti-retroviral treatment in order to protect his people from the toxic effects of
useless and harmful drugs, and to protect the country from indirect pillage by the vast
sums that are required to fulfil the anti-HIV-AIDS protocols, almost everyone rallied
against him, from local opposition to the corporate world of the IMF and the World
85

Bank. During that time CNN was broadcasting for Africa a very friendly and educative
World Bank advertisement about HIV-AIDS, informing everyone that HIV is the cause
of AIDS and how to treat it. We have not been shown that advertisement for the last two
years, ever since President Mbeki, out of intolerable political pressure, had to relinquish
his position and accept the introduction of anti-retroviral drugs like Nevirapine,
supposedly to protect his people from AIDS. Unfortunately President Mbeki had no
media group on his side to support him.

In the recent South African General Elections one of the electoral slogans was the
promise of ‘Free AIDS Drugs’. Knowing the cost of this, in lives and in resources, the
marketing scheme is in fact a cruel marketing scam.

At this point we must emphasise that there is no conspiracy sustaining all of this. Indeed,
no-one could ever orchestrate it. The phenomenon happens as a spontaneous emergence
of a common interest that coincides in a particular arena. The 1980-83 life-style
hypothesis of AIDS was not an adequate framework for any confluence of commercial,
political or personal interests. But with the 1984 launch of the viral hypothesis, the
perfect arena was created for, as it were, a spontaneous collusion of interests to emerge.
HIV as the cause of AIDS makes everything simple for everyone. Simple for R. Gallo,
who in 1984 claimed to have discovered HIV. The first thing he did was to patent the
HIV test. Simple for the pharmaceuticals corporations, who were already analysing the
business possibilities that the new HIV-AIDS hypothesis could bring by the marketing of
anti-retroviral drugs, tests and related pharmaceutical products. Simple for cancer
researchers on retroviruses, who faced dismal prospects for future grants in the cancer
field, but who suddenly became the new HIV-experts, eager to embrace the discovery of
HIV, make their mark, and grab one of the numerous grants now available for research
on HIV-AIDS. Simple for politicians, waiting to get their hands on anything that can get
them more votes, and 1984 was a re-election year for Ronald Reagan. The discovery of
HIV was boasted by the politicians as the discovery of the century, again another proud
American contribution to the advancement of science.

No-one has ever proven that HIV causes AIDS. No-one has ever produced definite
scientific evidence that HIV really exists. There are no major scientific journals without
corporate connections to the companies who make things for scientists to buy, and the
companies who make drugs for doctors to sell. If Montagnier and Gallo’s original
1983/84 scientific papers that claim to have identified HIV did not really find the
evidence, why was their work published? Since then, tens of thousands of scientists and
researchers have spent billions of dollars a year working on the idea contained in those
papers and endorsed by prestigious medical journals.
86

HIV as the cause of AIDS also made things easy for those medical practitioners who like
things clear and simple, and who were ready to support the reductionist new HIV-AIDS
hypothesis. When HIV was announced as the cause of AIDS in 1984, the Centres for
Disease Control requested that doctors should report any patients displaying certain
symptoms and test them for antibodies to this organism. The CDC’s report, intended for
physicians, did not identify any of the original work on the basis of which this clinical
protocol was being established. Physicians did not need to know the source of the
information, since any physician would assume that the CDC had real evidence and proof
that HIV was the cause of AIDS. The new, clear parameters to diagnose and treat what
was before a puzzling syndrome made everything easier. Now AIDS is an infectious
disease, diagnosed by the HIV-test and treated with anti-retrovirals.
Socially, HIV was the perfect scapegoat to disguise the evidence of the pathological
consequences of homosexual practices. The American and European homosexual lobby
unconditionally supported and promoted HIV, the virus that can attack ‘anyone’.
Suddenly everyone was at risk, exonerating them publicly from the consequences of their
unnatural practice. Also, with the fantasy of a viral disease, homosexual HIV-positives
were the first to rush to take AZT even before it was approved by the FDA (of course,
rumours of its wonders were spread during the AZT trials for FDA approval). And we
should not forget that among the other beneficiaries of the HIV-AIDS hypothesis, the
latex industry is booming with the manufacture of condoms.
As one insightful scientist has stated, “HIV is an entity of convenience that meets the
needs of powerful groups.”

We have to realise that what is happening is in the very nature of the capitalist ‘free
market’. Capitalism is evolutionism at work, the survival of the greediest and most
deceitful by economic selection. As the scorpion said to the frog, “I am sorry, but it is in
my nature, I have to sting you!” And that is the sting of capitalism, it is in its nature, one
might say a metabolic product of its organic function. As an organism, like the scorpion,
it produces venom. One of the toxic compounds in the venom of capitalism is usurious
money, which intoxicates every transaction happening in the world and pays for every
medical research taking place on the planet.

To take this metaphor further, the toxic effect of that particular compound (paper
money) is a progressive depletion of the wealth of the host, of the country of the host, of
the planet of the host. So wealth suppression is the destructive mechanism by which the
poison works. Like the immune-suppressive anti-retroviral drugs, it interferes with the
replication of the genetics of existence in the human transaction: justice, and just
transactions.

87
Its interference is by introducing a new artificial ‘gene pattern’ that blocks the replication
of justice within people’s transactions. The gene is the code for interest.
The toxic effect of the new protein, interest, by perpetuating unjust transactions,
becomes a norm and replaces the natural knowledge of ‘how to live’ which, in medical
terms, is called physiology, from physis: what is natural, and logos: knowledge, and
replaced by one that causes corruption on the earth. Once interest becomes natural, it
becomes pathological. When a human being, like any cell, stops knowing ‘how to live’, it
dies.

Thus interest, the chain-terminator of the existential natural pattern, like the DNA chain terminator AZT, finally destroys man by depleting him of power, of sovereignty,
territory, and meaning.
It is therefore no surprise to see that when the usurious gene that holds the code for
Interest parasitises  the market of pharmaceutical research, the result is the production of
a drug that poisons by prescription. It kills you, and you pay for the cost.
The phenomenon finally reveals itself (usury), from itself (toxicity), as itself (poisonous
drugs).

Categorically, we can say that any HIV-positive person, with AIDS symptoms or
without, is better off without anti-retrovirals.

The most recent stage of this business so far has been to export the whole package of
HIV-AIDS to Africa, India, China, and other countries where poverty is the common
denominator. HIV test, T-cell count and anti-retrovirals are an export of the USA. With
the test, old diseases are renamed, they now have a new cause, the new market has been
created, and the drugs are ready.
* * * * *
While the clarification of the African AIDS epidemic was the original question that led to
this report, scientific accuracy requires further explanation on the aetiological side.
88
Since we know that the HIV test is not a diagnostic tool for AIDS, its only use can be to
engender the world-wide epidemic of HIV-positives, the ‘HIV infected’ people,
recipients of anti-retroviral treatment and HIV-AIDS medical protocols. Medical data
becomes political when it is used in statistical projections by the international community
of financiers (IMF, World Bank, and others), forcing the African governments to accept
AIDS packages.
Besides the HIV-positive estimates, what we are left with in Africa are people with
diseases associated with immune deficiency.
It has been said before that tuberculosis, protein-calorie malnutrition and parasitic
diseases can all be associated with the depression of cellular immunity.(59)
A wide range of protozoal and helmintic infections prevalent in Africa have been
reported to induce immune deficiency.(60)
Africans, in certain areas, are endemically exposed to a wide variety of viruses, including
cytomegalovirus, Epstein-Barr virus and herpes simplex virus, all of which modulate the
immune system. Furthermore, other areas of Africa have a variety of endemic diseases
which have a major effect on the immune system, such as malaria, trypanosomiasis and
filariasis.(61)
We have described the African immune deficiency epidemic as being an epidemic of
poor, underdeveloped countries, and thus implied that poverty is the major factor
responsible for poor protein-calorie intake, poor water resources and sanitation, and
endemic intestinal parasitosis. All of the African governments are telling their electorates
that they are implementing development plans to reduce poverty.
We are forced to take our scientific inquiry further, because if we stop at poverty, we
risk allowing a major flaw in our thesis by misreading the evidence.
The statement made previously that there is an ‘AIDS of poor underdeveloped countries’
is not phenomenologically true if we move the scope of our focus out from the microelement
representing a poor child dying of malnutrition, and into the broader view of the
rich ground in which the dying child is going to be buried. He will be buried with all the
other underground natural wealth that still exists beneath the African soil.
89
The African countries may be underdeveloped in certain respects, and for certain people
(under the Apartheid regime, South Africa had developed an atomic bomb), but what
they are not is poor countries. That statement would be completely unscientific.
In any given pathological process we can identify primary and secondary causes.
Poverty means a lack of wealth, but the African countries are not poor countries with
poor natural resources. On the contrary, African countries have gold, diamonds,
platinum, oil, and so on, quite aside from their extensive fertile lands. We cannot
consider poverty to be the primary cause of the phenomenon, but rather the lack of
wealth of the majority of the individuals that display the poverty-defining diseases. This
is something completely different.
If the country has wealth, but a large proportion of its people suffer from povertydefining
diseases, we have to conclude that the wealth of the country does not reach the
source of the condition that creates the revealing diseases. A lack of distribution of
wealth could account for the impairment of economic life, and therefore the povertydefining
diseases.
In order to distribute wealth you first have to have ownership over it. Here this is the
case more than ever, since the wealth is under the feet of the people, but not in their
hands.
What this means is that between the extraction of the precious minerals from beneath the
ground, and the hands of the person—although this is a very small distance—the wealth
disappears.
Ultimately the disappearance of the wealth, by whatever means, and the unavailability of
it for the majority of the individuals living in the African continent, is the prima causa
morbo—that which causes the individual itself to reflect the consequences of wealth
impairment. One of the biological markers of this pathological situation [pathos: pain] is
the African immune deficiency epidemic of related diseases.
The physician’s highest mission—his only mission—is to restore the sick to health, to
‘cure’ as it is termed. And in order to find the cure, the doctor has to know first what
needs to be cured.
90
REFERENCES

1. Gallagher RE, Gallo RC. (1975). Type C RNA Tumor Virus Isolated from Cultured Human Acute Myelogenous
Leukemia Cells. Science 187:350-353.
2. Gallo RC, Wong-Staal F, Reitz M, Gallagher Re, Miller N, Gillespie DH. Some evidence for infectious type-C
virus in humans. (1976). p. 385-405 In: Animal Virology Baltimore D, Huang AS, Fox CF, eds Academic Press
Inc., New York.
2b. Poiesz BJ, Ruscetti FW, Gazdar AF et al: Detection and isolation of type C retrovirus particles from fresh and
cultured lymphocytes of a patient with coetaneous T-cell lymphoma. Proc. Natl Acad Sci USA 77:7415, 1980.
2c. Gallo RC: Human T-cell leukaemia-lymphoma virus andT-cell malignancies in adults. Cancer Surv 3:113, 1984
3. Snyder HW, Fleissner E. (1980) Specificity of human antibodies to oncovirus glycoproteins: Recognition of
antigen by natural antibodies directed against carbohydrate structures. Proc. Natl. Acad. Sci. USA 77:1622-1626
4. Barbacid M, Bolognesi D, Aaronson SA. (1980). Humans have antibodies capable of recognizing oncoviral
glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins
rather than as consequence of exposure to virus. Proc. Natl. Acad. Sci. USA 77: 1617- 1621.
5. Barré-Sinoussi F, Chermann JC, Rey F. (1983). Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk
for Acquired Immune Deficiency Syndrome (AIDS). Science 220:868-871.
6. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection, Isolation, and Continuous Production of
Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 224:497-500.
7. Sinoussi F, Mendiola L, Chermann JC. (1973). Purification and partial differentiation of the particles of murine
sarcoma virus (M, MSV) according to their sedimentation rates in sucrose density gradients. Spectra 4: 237- 243.
8. Toplin I. (1973). Tumor Virus Purification using Zonal Rotors. Spectra 4:225-235
9. Frank H. Retroviridae. (1987). p.253-256 In: Animal Virus and Structure, Nermut MV, Steven AC, eds Elsivier,
Oxford.
10. Papadopulos-Eleopulos E, Turner VF, Papdimitriou JM. (1993). Is a Positive Western Blot Proof of HIV
Infection? Bio/Technology 11(June): 696-707.
11. Gelderblom HR, Özel M, Hausmann EHS, Winkel T, Pauli G, Koch MA. (1988). Fine Structure of Human
Immunodeficiency Virus (HIV), Immunolocalization Of Structural Proteins And Virus-Cell Relation. Micron
Microscopica 19:41-60.
12. Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. (1997). Cell membrane vesicles are a major
contaminant of gradient-enriched human immunodeficiency type-1 preparations. Virol.230: 125-133.
13. Bess JW, Gorelick RJ, Bosche Wj, Henderson LE, Arthur LO. (1997). Microvesicles are a source of
contaminating cellular proteins found in purified HIV-1 preparations. Virol. 230: 134-144.
14. Levy JA. (1996). Infection by human immunodeficiency virus-CD4 is not enough. NEJM 335: 1528-1530.
15. Wong-Staal F, Hahn B, Manzuri V, et al. (1983). A survey of human leukaemias for sequences of a human
retyrovirus. Nature 302: 626-628.
91
16. Weissbach A, Baltimore D, Bollum F. (1975). Nomenclature of eukaryotic DNA polymerases. Science 190:
401-402.
17. O’Hara CJ, Groopmen JE, Federman M. (1988). The Ultrastructural and Immunohistochemical Demonstration
of Viral Particles in Lymph Nodes from Human Immunodeficiency Virus-Related Lymphadenopathy Syndromes.
Human Pathology 19:545-549.
18. Berzofsky JA, Berkower IJ, Epstein SL. Antigen-Antibody Interactions and Monoclonal Antibodies. (1993).
p.421-465 In: Fundamental Immunology Paul WE, ed 3rd ed Raven, New York.
19. Owen M, Steward M. Antigen recognition. (1996). p.7.1-7.12 In: Immunology Roitt Brostoff J, Male D, eds, 4th
ed Mosby, London.
20. BIO-RAD, 1989. Instruction manual of a Western Blot kit manufacturer.
21. Ratner L, Haseltine W, Paterca RP. et al (1985). Complete nucleotide sequence of the AIDS virus, HTLV-III.
Nature 313: 277-284.
22. Henderson LE, Sowder R, Copeland TD. et al. (1987). Direct Identification of Class II Histocompatibility DR
Proteins in Preparations of Human T-Cell Lymphotropic Virus Type III. J. Virol. 61:629-632.
23. Papadopulos-Eleopulos E. Turner Vf, Papadimitriou JM. (1992) Oxidative stress, HIV and AIDS. Res.
Immunol. 143:145148.
24. Hinshaw DB, Burger JM, Beals TF, et al. (1991) Actin polymerization in cellular oxidant injury. Arch.
Biochem. Biophys. 228: 311-316.
25. Bach MA, Lewis DE, McClure JE, et al. (1986). Monoclonal Anti-actin Antibody Recognizes a Surface
Molecule on Normal and Transformed Human B-lymphocytes: Expression Varies with Phase of Cell Cycle. Cell
Immunol. 98: 364-374.
26. Stricker RB, Abrams DI, Corash L, et al. (1985). Target Platelet Antigen in Homosexual Men with Immune
Thrombocytopenia. NEJM 313:1375-1380.
27. Wong-Staal F, Gallo RC. (1985). Human T-lymphotropic retroviruses. Nature 317: 395-403.
28. Genesca J, Jett BW, Epstein JS, et al. (1989) What do Western Blot indeterminate patterns for Human
Immunodeficiency Virus mean in EIA-negative blood donors? Lancet II: 1023-1025.
29. Ranki A, Johansson E, and Krohn K (1988), Interpretation of Antibodies Reacting Solely with Human
Retroviral Core Proteins. NEJM 318: 448-449.
30. Wilber JC. (1991) New Developments in Diagnosing Infections, p.1-15. In: AIDS Clinical Review. P.
Volbering, MA. Jacobson (Eds). Marcel Dekker Inc. New York.
31. Lundberg GD. (1988). Serological Diagnosis of Human Immunodeficiency Virus Infection by Western Blot
Testing. JAMA 260:674-679.
32. Pinter A, Honnen WJ, Tilley SA. et al. (1989). Oligomeric Structure of gp41, the Transmembrane Protein of
Human Immunodeficiency Virus Type 1. J. Virol. 63: 2674-2679.
33. Burke DS. (1989). Laboratory Diagnosis of Human Immunodeficiency Virus Infection. Clin. Lab. Med. 9:369-
392.
92
34. Maskill WJ, Gust ID. (1992). HIV-1 Testing in Australia. Australian Prescriber 15:11-13.
35. Conley Cl, Savarese D. (1989). Biologic False-Positive Serologic Tests for Syphilis and Other Serologic
Abnormalities in Autoimmune Haemolytic Anemia and Thrombocytopenic Purpura. Medicine 68:67-84.
36. Boue F, Dreyfus M, Bridley F, et al. (1990). Lupus anticoagulant and HIV infection: A prospective study. AIDS.
4:467-471.
37. Jaffe JH, Moore JD, Cone EJ, et al. (1986). HTLV-III Seropositivity in 1971-1972 Parenteral Drug Abusers. A
case of false Positives or Evidence of Viral Exposure? NEJM 314:1387-1388.
38. Physicians Desk Reference (PDR). Nevirapine (Viramune-Roxane). 55 Edition. Montuale NJ. Medical
Economics Company, Inc. 2001. p.2838-2842.
39. Ternynck T, Avrameas S. (1986) Murine Natural Monoclonal Autoantibodies: A study of their Polyspecificities
and their Affinities, Immunol. Rev. 94: 99-112.
40. Pateraki E, Kaklamani E, Potocalas KR, et al. (1986). Autoantobodies in systemic lupus erythematosus and
normal subjects. Clin. Rheumatol. 5:338-345.
41. Essex M, Mclane MF, Lee TH. et al. (1983). Antibodies to Cell Membrane Antigens Associated with Human
T-Cell Leukaemia Virus in Patients with AIDS. Science 220: 859-862.
42. Beneviste RE, Ochs HD, Fischer SH. et al. (1986). Screening for antibodies to LAV/HTLV-III in recipients of
immunoglobulin preparations. Lancet I:1090-1092.
43. Burinsky KI, Chaplinskas SA, Syrtsev VA. et al. (1988). Reactivity to gag- and env-related sequences in
immunoblot assay is not necessarily indicative of HIV infection. AIDS 2:405-406.
44. Matsiota P, Charmaret S, Montagnier L. et al. (1987). Detection of Natural Autoantibodies in the serum of
Anti-HIV Positive-Individuals. Ann. Inst. Pasteur/Immunol. 138: 223-233.
45. Calabrese LH. (1988). Autoimmune Manifestations of Human Immunodeficiency Virus (HIV) Infection. Clin.
Lab. Med. 8: 269-279.
46. Lucey DR. Hendrix CW, Andrzejewski C. et al. (1992). Comparison by Race of Total Serum IgG, IgA, and IgM
with CD4+ T-Cell Counts in North American Persons Infected with Human Immunodeficiency Virus Type 1. J.
Acquir. Immun. Defic. Syndr. 5:325-332.
47. Rodriguez L, Dewhurst S, Sinangil F. et al. (1985). Antibodies to HTLV-III/LAV among Aboriginal Amazonian
Indians in Venezuela. Lancet II: 1098-1000.
48. Volsky DJ, Wu YT, Stevenson M. et al. (1986). Antibodies to HTLV-III/LAV in Venezuelan patients with acute
malarial syndromes. NEJM 314: 647.
49. Gallo RC, Sarin PS, Wu AM. (1973). On the nature of the Nucleic Acids and RNA Dependent DNA
Polymerase from RNA Tumor Viruses and Human Cells, p.13-34. In: Possible Episomes in Eukaryotes. LG
Silvestri (ed.). North-Holland Publishing Company, Amsterdam.
50. Whitkin SS, Higgins PJ, Bendich A. (1978) Inhibition of reverse transcriptase and human sperm DNA
polymerase by anti-sperm antibodies. Clin.Exp.Immunol. 33: 244-251.
51. Tomley FM, Armstrong SJ, Mahy BWJ, Owen LN, (1983). Reverse transcriptase activity and particles of
retroviral density in cultured canine lymphosarcoma supernatants. Br.J.Cancer 47: 277-284.
93
52. Weissbach A, Baltimore D, Bollum F. et al (1975). Nomenclature of Eukaryotic DNA Polymerases. Science
190: 401-402.
53. Panem S, Prochownik EV, Reale FR. et al. (1975). Isolation of Type-C Virions from Normal Human Fibroblast
Strain. Science 189: 297-299.
54. Panem S, Prochownik EV, Kniish WM, Kirsten WH. (1977). Cell Generation and Type-C Virus Expression in
the Human Embryonic Cell Strain HEL-12. J. Gen. Virol. 35: 484-495.
55. Panem S, (1979) C Type Virus Expression in the Placenta. Curr.Top.Pathol. 66: 175-189.
56. Weiss RA, Friis RR, Katz E. et al. (1971). Induction of Avian Tumor Viruses in Normal Cells by Physical and
Chemical Carcinogens. Virol. 46: 920-938.
57. Temin HM. (1974). On the origen of RNA Tumor Viruses. Harvey Lect. 69: 173-197.
58. Nakamura N, Sugino H, Takahara K. et al. (1991). Endogenous retroviral LTR DNA sequences as markers for
individual human chromosomes. Cytogenet. Cell Genet. 57: 18-22.
59. Gruest J, Barre-Sanoussi F, Geroldi D, Chermann JC, McCormick J, Mitchell S, Piot P, Taelman H, Mirlangu
KB, Wobin O, et al.(1984). Prevalence of antibodies to lymphadenopathy-associated retrovirus in African patients
with AIDS. Science 226: 453-456.
60. Clumeck N, Sonnet J, Taelman H, Mascart-Lemone F, de Bruyere D, Vandeperre P, et al. (1984). Acquired
immunodeficiency syndrome in African patients. New England Journal of Medecine 310: 492-487.
61. Biggar RJ. (1986). The AIDS problem in Africa.
62. Quinn TC, Piot P, McCormick JB, Feinsod FM, Taelman H, Kapita B, Stevens W, Fauci AS. (1987). Serologic
and immunologic studies in patients with AIDS in North America and Africa. Journal of the Amarican Medical
Association 257: 2617-2621.
63. WHO. (1986) Acquired Immunodeficiency Syndrime (AIDS). WHO/CDC case definiton for AIDS. Weekly
Epidemiology Record 61: 67-76.
64. Mann JM, Francis H, Quinn T, Asila PK, Bosenge N, Nzilambi N, Bila K, Tamfum M, Ruti K, Piot P,
McCormick J, Curran JW. (1986). Surveillance for AIDS in a central African city. Journal of the American Medical
Association. 255: 3255-3259.
65. Kashala O, Marlink R, Ilunga M, Diese M, Gormus B, Xu K, Mukeba P, Kasongo K, Essex M. (1994).
Infection with human immunodeficiency virus type 1 (HTV-1) and human T-cell lymphotropic viruses among
leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan.
Journal of Infectious Diseases. 169: 296-304.
66. Van De Pierre P, Lepage P, Kestelyn P, Hekker AC, Rouvroy D, Bogaerts J, Kayihigi J, Butzler JP, Clumock N.
(1984). Acquired Immunodeficiency Syndrome in Rwanda. Lancet II: 62-65.
67. Nzilambi N, Mann JM, Francis H. (1986). Seroprevalence among tuberculosis patients in Zaire. In: Abstracts II
International AIDS Conference. No. 105: S17b. Paris.
68. European Study Group. (1989). Risk factors for male to female transmission of HIV. British Medical Journal.
298: 411-414.
94
69. Kingsley LA, Kaslow R, Rinaldo CR, Detre K, Odaka N, Van Raden M, Detels R, Polk BF, Chmiel J, Kesley
SF, Ostrow D, Visscher B. (1987) Risk factors for seroconversion to human immunodeficiency virus among male
homosexuals. Lancet I, 345-348.
70. Stevens CE, Taylor PE, Zang EA, Morrison JM, Harley EJ, de Cordoba Sr, Bacino C, Bodner AJ, Sarngaharan
MG, Gallo RC, Rubinstein P. (1986). Human T-cell lymphotropic virus type III infection in a cohort of homosexual
men in New York City. Journal of the American Medical Association, 255: 2167-2172.
71. Ameisen J, Capron A. (1991). Cell dysfunction and depletion in AIDS: The programmed cell death hypothesis.
Immunol. Today 12: 102-105.
72. Klatzmann D, Montagnier L. (1986). Approaches to AIDS therapy. Nature 319: 10-11.
73. Lemaitre M, Guetard D, Henin Y, Montagnier L, Zerial A. (1990). Protective activity of tretracycline analogs
against the cytopathic effect of the human immunodeficiency viruses in CEM cells. Res. Virol. 141: 5-16.
74a. Papadopulos-Eleopulos E. (1982). A Mitotic Theory. J.Theor. Biol. 96: 741-758.
74b. Papadopulos-Eleopulos E, Turner VF. Papadimitriou JM. (1992). Oxidative Stress, HIV and AIDS. Res.
Immunol. 143: 145-148
75. Kerr JFR, Searle J. (1972). A Suggested Explanation for the Paradoxically Slow Growth Rate of Basal-Cell
Carcinomas that Contain Numerous Mitotic Figures. J. Pathol. 107: 41-45.
76. Don MM, Ablett G, Bishop Cj, Bundesen PG, Donald KJ, Dearle J, Kerr JFR. (1977). Death of Cells by
Apoptosis Following Attachment of Specifically Allergized Lymphocytes In Vitro. Aust. J. Exp. Biol. Med. Sci. 55:
407-417.
77. Wyllie AH, Kerr JFR, Currie AR. (1980). Cell Death: The Significance of Apotosis. Inernat. Rev. Cytol. 68:
251-306.
78. Wyllie AH, Morris RG, Smith AL, Dunlop D. (1984) Chromatin Cleavage in Apotosis: Association with
Condensed Chromatin Morphology and Dependence on Macromolecular Synthesis. J. Pathol. 142: 67-77.
80. Cohen JJ, Duke RC. (1984). Glucocorticoid Activation of a Calcium-Dependent Endonuclease in Thymocyte
Nuclei Leads to Cell Death. J. Immunol. 132: 38-42.
81. McConkey DJ, Hartzell P, Duddy SK, Hakansson H, Orrenius S. (1988). 2,3,7,8-Tetrachlorodibenzo-p-dioxin
Kills Immature Thymocytes by Ca2+-Mediated Endonuclease Activation. Science.
82. McConkey DJ, Hartzell P, Amador-Perez JF, Orrenius S, Jondal M. (1989) Calcium-Dependent Killing of
Immature Thymocytes by Stimulation via the CD3/T Cell Receptor Complex. J. Immunol. 143: 1801-1806.
83. Reed DJ. (1990) Status of Calcium and Thiols in Hepatocellular Injury by Oxidative Stress. Seminars in Liver
Disease. 10: 285-292.
84. Trimm JL, Salama G, Abramson JJ. (1986) Sulphydryl Oxidation Induces Rapid Calcium Release from
Sarcoplasmic Reticulum Vesicles. J. Biol. Chem. 261: 16092-16098.
85. Rene O, Dragic T, Lopez O, Herzenberg L, Montagnier L. (1992). An Anti-Oxidant Prevents Apoptosis and
Early Cell Death in Lymphocytes from HIV Infected Individuals. Volume 2, pp. A65 in: VIIIth International
Conference on AIDS, Amsterdam.
95
86. Montagnier L. (1985). Lymphadeneopathy-Associated Virus: From Molecular Biology to Pathogenicity. Ann.
Int. Med. 103: 689-693.
87. Laurent-Crawford AG, Krust B, Muller S. Riviere Y, Rey-Cuille MA, Behet JM, Montagnier L, Hovanessian
AG. (1991). The Cytopathic Effect of HIV is Associated with Apoptosis. Virol. 185: 829-839.
88. Des Jarlais DC, Friedman SR, Marmor M, Mildvan D, Yancovitz S, Sotheran JL, Wenston J, Beatrice S.
(1993). CD4 lymphocytopenia among injecting drug-users in New York City. J. Acquir. Immune Defic. Syndr. 6:
820-822.
89. Nicolosi A, Musico M, Saracco A, Molinari S, Ziliabi N, Lazzarin A. (1990). Incidence and risk factors of HIV
infection: A prospective study of seronegative drug-users from Milan and Northern Italy, 1987-1989. Epidemiology
1: 453-459.
90. Detels R, English PA, Giorgi JV, Visscher BR, Fahey JL, Taylor JMG, Dudley JP, Nishanian P, Muñoz A,
Phair JP, Polk BF, Rinaldo CR. (1988) Patterns of CD4+ Cell Changes after HIV-1 Infection Indicate the Existence
of a Codeterminant of AIDS. J. Acquir. Immune. Defic. Syndr. 1: 390-395.
91. Margolick JB, Donnenbery AD, Muñoz A, Park LP, Bauer KD, Giorgi JV, Ferbas J, Saah AJ. (1993). Changes
in T and Non-T-lymphocyte Subsets Following Seroconversion to HIV-1: Stable CD£+ and Declining CD3-
Populations Suggest Regulatory Resposes Linked to loss of CD4 Lymphocytes. J. Acquir. Immune. Defic. Syndr. 6:
153-161.
92. Adlemann LM, Wofsy D. (1993). T-Cell Homeostasis: Implications in HIV Infection. J. Acquir. Immune. Defic.
Syndr. 6: 144-152.
93. Stanley SK, Fauci AS. (1993) T Cell Hoeostasis in HIV Infection: Part of the Solution, or Part of the Problem?
J. Acquir. Immune. Defic. Syndr. 6: 142-143.
94. Burns CF, Battye FL, Goldstein G. (1982). Surface Antigen Changes Ocurring in Short-Term Cultures of
Activated Human T-lymphocytes: Analysis by Flow Cytometry. Cell. Immunol. 71: 12-26.
95. Zagury D, Bernard J, Morgan DA, Fouchard M, Feldman M. (1983). Phenotypic Diversity within Clones of
Human Normal T Cells. Int. J. Cancer. 31: 705-710.
96. Lamoureux G, Davignon L, Turcotte R, Laveriere M, Mankiewicz E, Walker MC. (1987). Is Prior
Mycobacterium Infection a Common Predisposing Factor to AIDS in Haitians and Africans? Ann. Inst.
Pasteur/Immunol. 138: 521-529.
97. Fauci AS. (1988). The Human Immunodeficiency Virus: Infectivity and Mechanisms of Pathogenesis. Science
239: 671-622.
98. Pantaleo G, Graziosi C, Fauci AS. (1993). The Immunopathogenesis of Human Immunodeficiency Virus
Infection. NEJM. 328: 327-335.
99. Volsky DJ, Wu YT, Stevenson M, Dewhurst S, Sinangil F, Merino F, Rodriguez L, Godoy G. (1986).
Antibodies to HTLV-III/LAV in Venezuelan Patients with Acute Malarial Syndromes. NEJM. 316: 647-648.
100. Hoover DR, Saah AJ, Bacellar H, Murphy R, Visscher B, Anderson R, Kaslow RA. (1993). Signs and
symptoms of “asymptomatic” HIV-1 infection in homoxsexual men J. Acquir. Immune. Defic. Syndr. 6: 66-71.
96
101. Ludlam CA, Steel CM, Cheingsong-Popov R, McClelland DBL, Tucker J, Tedder RS, Weiss RA, Philip I,
Prescott RJ. (1985). Human T-Lymphotropic Virus Type-III (HTLV-III) Infection in Seronegative Haemophiliacs
after Transfusion of Factor VIII. Lancet II: 233-236.
102. Shu-Chun et al. Retrotransposon reverse-transcriptase-mediated repair of chromosomal breaks. Nature Vol
328, 641-644. Oct. 1996.
103. Dourmashkin RR, O'Toole CM, Bucher D, Oxford JS. The presence of budding virus-like particles in human
Lymphoid cells used for HIV cultivation. VIIth International Conference on AIDS. Florence: 1991: 122.
104. Widy-Wirski R, Berkley S, Downing R, Okware S, Recine U, Mugerwas R, Lwegaba A, Sempala S. 1988:
Evaluation of the WHO clinical case definition for AIDS in Uganda. JAMA 260: (22) 3286-3289.
105. WHO, Weekly Epidemiological Record 73, 373-380 (1998). UNAIDS, Dec. 1999: AIDS epidemic update.
106. P Duesberg, C Koehnlein, D Rasnick. The chemical bases of the various AIDS epidemics: recreational drugs,
anti-viral chemoterapy and malnutrition. J. Biosci. Vol 28, no.4, June 2003.
107. Levy JA, Hoffman AD, Kramer SM, Landis JA, Shimabukuro JM, 1984. Isolation of lymphocytopathic
retroviruses from San Francisco patients with AIDS; Science 225 840-842.
108. Simmonds P, Balfe P, Peutherer JF, Ludlam CA, Bishop JO, Leigh-Brown AJ 1990, Human immunodeficiency
virus-infected individuals contain provirus in small numbers of peripheral mononuclear cells and at low copy
numbers. J. Virol. 64 864-872.
109. Eleni Papadopulos-Eleopulos. Is HIV the cause of AIDS? 1997. Continuum.
110. Hoxie JA, Haggarty BS, Rakowski JL, Pillsbury N, Levy JA. 1985. Persistent noncytopathic infection of
normal human T-lymphocytes with AIDS-associated retrovirus; Science 229, 1400-1402.
111. McCune JM 2001. The dynamics of CD4+ T-cell depletion in HIV disease: Nature 410, 974-979.
112. Padian NS, Shiboski SC, Glass SO, Vittinghoff E. Heterosexual transmission of HIV in northern California:
results from a ten year study. Am. J. Epdemio. 1997; 146:350-7.
113. Duesberg PH, Rasnick D. 1998. The Aids dilemma: drug diseases blamed on a passenger virus. Genetica 104:
85-132.
114. Furman PA, Fyfe JA, Clair MST, Weinhold K, Rideout JL, Freeman GA, Nusinoff S, Bolognesi DP, Broder S,
Mitsuya H, Barry DW. 1992. Phosphorilation of 3'azido 3'deoxythymidine and Selective Interaction of the
5'triphosphate with Human Immunodeficiency Virus Reverse Transcriptase. Proceedings of the National Academy
of Sciences. 83: 8333-8337.
115. Fischl MA, Richman DD, Grieco MH, Gottlieb MS, Volberding PA, Laskin OL, Leedon JM, Groopman JE,
Mildvan D, Schooley RT, Jackson GG, Durack DT. King D. 1987. The Efficacy of Azidothymidine (AZT) in the
Treatment of Patients with AIDS and AIDS-Related Complex. New England Journal of Medicine. 317: 185-191.
116. Rasnick D. 1997. Kinetics analysis of consecutive HIV proteolytic cleavages of the Gag-Pol polyprotein. J.
Biol. Chem. 272. 6348-6353.
117. Roit IM, Brostoff J, Male DV. (1991). Immunology. Gower Medical Publishing, UK.
118. Ludiam CA, Steel CM, Cheingsong-Popov R, et al. (1985) Human T-Lymphotropic Virus Type-III (HTLV-III)
Infection in Seronogative Haemophilliacs after Transfusion of Factor VIII. Lancet II:233-236
97
119. Kingsley LA, Kaslow R, Rinaldo CR, et al. (1987). Risk factors for seroconversion to human
immunodeficiency virus among male homosexuals. Lancet I: 345-348.
120. Goedert JJ, et al. (1982). Amyl Nitrate may alter T-lymphocytes in homosexual men. Lancet 2: 412.
121. Fauci SA, et al. (1984) Acquired immunodeficiency syndrome; Epidemiologic, clinical, immunologic, and
therapeutic considerations. Ann. Intern.Med. 100: 92
122. Finch R. (1980). Immunomodulating effects of antimicrobial agents. J. Antimicrob. Chemother. 6: 691.
123. Papadopulos-Eleopulos E. (1988). Reappraisal of AIDS- Is the Oxidation induced by the risk factors the
primary cause?. Medical Hypotheses. 25. 151-162.
124. Jacob L. et al. 1986. Possible genetic susceptibility to the acquired immunodeficiency syndrome in
hemophiliacs. Ann. Intern. Med. 104:130.
125. Vilmer E, et al. 1984. Isolation of new lymphotropic retrovirus from two siblings with haemophilia B, one
with AIDS. Lancet 1: 753.
126. Connor EM, et al. 1994. Reduction of Materna-Infant transmission of HIV type 1 with Zidovudine treatment.
N. Engl. J. Med.331: 1173-1180.
127. Robert Gallo. The First Human Retrovirus. Scientific American. December. 1986
128. Shepard RN, Schock J, Robertson K, et al. 2000. Quantitation of human immunedeficiency virus type 1 RNA
in different biological compartments. Journal of Clinical Microbiology 38: 1414-8.
129. Gayle H. 2000. An overview of the global HIV/AIDS epidemic, with a focus on the United States. AIDS 14
Suppl. 2:S8-17.
130. Schuerman L, Seynhhhhaeve V, Bachschmidt I, Tchotch V et al. 1988. Severe malnutrition and paediatric
AIDS: a diagnositic problem in rural Africa. AIDS 2:232-3.
131. Kumar and Clarke. 1999. Clinical Medicine, fourth edition. W.B. Saunders
132. The European Collaborative Study. 1988. Mother-to-child transmission of HIV infection. Lancet II:1039-1043.
133. CDC. 1982 Unexplained immunodeficiency and opportunistic infections in infants—New York, New Jersey,
California. Morbidity and Mortality Weekly Reports 31: 665-7.
134. Oleske J, Minnefor A, Cooper R, et al. 1983. Immune deficiency with reversed T4/T8 ratios in infants born to
promiscuous and drug-addicted mothers. Journal of the American Medical Association. 249:2350-6.
135. Rogers MF, Ou CY, Rayfield M et al. 1989. Use of polymerase chain reaction for early detection of the
proviral sequences of human immunodeficiency virus in infants born to seropositive mothers. New York City
Collaborative Study of Maternal HIV Transmission and Montefiore Medical Center HIV Perinatal Transmission
Study Group. New England Journal of Medicine 320: 1649-54.
136. Cowan MJ, Hellmann D, Chudwin D, Wara DW, Chang RS, Ammann AJ. 1984. Maternal transmission of
acquired immune deficiency syndrome. Pediatrics 73:382-6.
137. Thiry L, Sprecher-Goldberger S, Jonckheer T, et al. 1985. Isolation of AIDS virus from cell-free breast milk of
three healthy virus carriers. Lancet II:891-2.
98
138. Dunn DT, Newell ML, Ades AE, Peckham CS.1992. Risk of human immunodeficiency virus type 1 in breast
milk. Journal of Infectious Diseases.
139. Nicoll A, Timaeus I, Kigadye RM, Walrraven G, Killewo J. 1994 The impact of HIV-1 infection on mortality
in children under 5 years of age in sub-Saharan Africa: a demographic and epidemiologic analysis. AIDS 8:995-
1005.
140. Lusher JM, Operskalski Ea, Alerdort LM, et al. 1991. Risk of human immunodeficiency virus type-1 infection
among sexual and nonsexual household contacts of persons with congenital clotting disorders. Pediatrics 88:242-9.
141. Lower R, Lower J, Kurth R. 1996. The viruses in all of us: Characteristics and biological significance of
human endogenous retrovirus sequences. Proceedings of the National Academy of Sciences of the United States of
America 93:5177-84.
142. Rich JD, Merriman NA, Mylonakis E et al. 1999. Misdiagnosis of HIV by HIV-1 plasma viral load testing: A
case series. Annals of Internal Medicine 130:37-39.
143. Guay LA, Musoke P. Fleming T, et al. 1999. Intrapartum and neonatal single-dose nevirapine compared with
zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda. Lancet 354:795-802.
144. Cheeseman SH, Havlir D, McLaughlin MM, et al. 1995. Phase I/II evaluation of nevirapine alone and in
combination with zidovudine for infection of immunodeficiency virus. Journal of the Acquired Immmune Deficiency
Syndromes and Human Retrovirology 8:141-51.
145. Havlir D, Cheeseman SH, Mclaughlin MM, et al 1995. High-dose nevirapine: safety, pharmacokinetics, and
antiviral effect in patients with human immunodeficiency virus infection. Journal of Infectious Diseases: 171: 537-
45.
146. Papadopulos-Eleopulos E, Turner VF, Papadimitrion JM, Alfonso H, Page BAP, Causer D, Mhlongo S, Fiala
C, Miller T, Brink A Hodgkinson N. 2001. Mother to Child Transmission of HIV and its Prevention with AZT and
Nevirapine. A critical analisis of the evidence. The Perth Group, Perth, Western Australia.

 

 

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Hijriah Date

Jamadil Akhir
8
Saturday
1439 HIJRAH

Articles

Supreme Existence
God And Allah. Updated
The Meaning Of Life
Freedom Means Responsibility
Sovereignty
This Earth Is Precious
Qur'anic Caliphate
The Truth
Human Energy
Spiders
Seeds
Spiritual Evolution.
The Five Pillows Of Islam.
Salat (Desire)
Contemplation.
The Blinding Light Of Islam Extinguished.
Islam Demands Reason.
Believers.
Islamic Finance.
The Unnecessary Energy Crisis: How to Solve It Quickly.
Time Explained.
The Misanthrope.
The HIV-AIDS Question.
INDUCTION AND EXTREME OATH OF THE JESUITS
A Debate On Money.
Chaos Transduced.
The Advent Of The Muslims.
Islam A Challenge To Religion.
Sweet Poison.
The Three Given Keys Of Existence.
Divine Spark.
The Heavens The Earth And The Qur’an.
Mohammad's Awakening.
The Engines of Creation.
Dua.
Hamd.
Iblis.
Rage.
A Dying Ember
Melded Multiple Infinities.
A Sadness Within Me.
The Dichotomy of humanity; the singular unity of being both Mortal and Immortal.
Salaam.
Saum.
Shirk.
The purpose of humanities creation.
Interface With Islam
The potentials of Death.
Why the banks are failing.
The Subjugated Mind.
Allodial Earth.
THE BEGINNING OF THE LIE
CHAPTER 6 from the book "DESCENT into SLAVERY”
The Vatican.
Theft: Punishment or Relief
Love.
I’bada
Life.
The Fractional Reserve Banking System.
COSMOS WITHOUT GRAVITATION
The Symbols of Religion.
The Big Bang, a BIG lie.
The formation of a galaxy, evolving a universe.
Our Conscious Mind As An Electromagnetic Field
THE GEOMETRY OF SPACE
Hadith (part one).
Hadith Continued (part two).
Confessions Of English Spy Who Helped create Wahhabism.
The Detached.
Law of Men. (The First Crusade)
Rex Offa of Albien (Britain)
Constitution of Allah. Transfinite Consciousness.
PENTECOSTALISM.
THE REAL REASON WHY WOMEN HAVE BEEN OPPRESSED
The Human Soul Nexus.
The History of Arabic Grammar.
Why do the Innocent suffer, the answer.
A Careful Linguistic Analysis of the term Allah.
I skipped, and I danced, and I sang.
I am.
Who destroyed Alexandria Library?
The Empty Vessel.
Islam: What is the Quran and Sunnah? (Written in Arabic)
The Lie of Hijab. (Written in Arabic)
Human Energy Economic System.
Aspartame is Rumsfeld's Disease: A Politically-Induced Biochemical Disaster Of Global Proportions.
Polycentric Community.
Establishing Freedom of Evil at all Times within Bonded Community
Sovereignty is with Allah alone
University community model.
190 Lughaat-ul-Qur'an
Islamic Supermarket
COMPLAINTS OF CONVERTS
Car Insurance.
Islamic repository
The Skill of Discourse
The Natural Rights Clothes Shop
Meanings of Terms of law
A simple Lexicon investigation of a single verse of the Qur'an
The Nature of Ownership.
Police State: What is a police Officer?
Free Energy Plasma Engine
Riba
Part One. The Writ
Part Three: Gemot Administrators of Terrente (the peace of their mind threatened) Relief
Part Four - Wite and Surety Bound-Souls
Eight point community plan
Equitable Allodial Utilisation (overview)
Proposed Method of Allodium Witnessed Declaration
Affidavit of Allodium Witnessed Declaration
‘Bona Gestura’ Bond of Allodarii
Notice of pursuance of Allodium Witnessed Declaration
Declaration of Allodial Utilisation
Polycentric community (overview)
The Substantive Binding Surety (overview)
Reciprocated Agreement of Binding Surety
Anarchic Labour Trading
The Repository (overview)
Bonded Cooperative Occupational System
Plenary Allodium Utilisation Averment
Cooperative Assurance System
Cooperative Car Assurance
Medical Assurance
Winters slave
The Nature of War
The Nature of Democracy
The Nature of Sovereignty
The Third State of Consciousness
Inherent Power (short overview)
Part Two: How a Substantive Gemot of Axiological Inherent Power Functions through Axioms of the Land
Part Five - Terrente - Duty of Care - Outcast
The Law, Courts and Jurisdiction
Repository Securities and Advance
The Nature of Copyright
The Nature of Government
The Nature of Capitalism
Islamic Banking
The Court System versus the Witena-Gemot System
A Duty of Care
The Trivium
The Concept and Structure of Polycentric community
The Nature of Economics
The Protected Paedophiles, Child Rapists, Child Torturers, and Child Murders of the British Establis
Arbitration of Universal Accountability - Terrente Relief
Unilateral Bond of Repository Administrator
The Nature of the Hospital System
Hemp Drugs Commission Report, completed in 1894
Unlawful Killing
A Bonded Militia
Duty of Care Trading Declaration (food)
Bonded Cooperative Networks
Freedom or Slavery
Matrimonial Agreement
Part Six - Relief, Recourse and the Jury
Part Seven - Constructive versus Substantive
The Education Assurance Bond
Predator and Prey
Francis of Assisi
Possession versus Utilisation of the Land
NOTICE: No Implied or inferred right of access
Crowd Funding
The Master of the Soul
The Nature of Money
What is voting?
What is a Citizen?
Homeless
As Above so Below
Fencing (Austerity)
Jews and the Global Sex Slavery Business
Rise of Sea Levels is 'The Greatest Lie Ever Told'
The Nature of Death
The Singing Soul