DID DR. GALLO AND HIS COLLEAGUES MANIPULATE THE "AIDS-TEST" TO ORDER?
"The hunt for the virus" 1 has degenerated into "clean torture with fatal
result" 2
By Heinrich Kremer
Continuum Summer 1998
Who, for given reasons given below casts doubt
on the theory that "HIV causes AIDS", is often confronted with the
question,
if it did not, how is it that a patient who has been diagnosed as "HIV
positive" by the test sooner or later goes on to develop AIDS? To which
the AIDS sceptic usually replies that a "HIV-positive" laboratory result,
an arbitrary defined characteristic is part of the clinical diagnosis
"AIDS".
This exchange does not advance the argument
very much as to whether "AIDS" and "HIV" are scientifically-speaking
biological
entities and if between them a biological cause-effect relationship is
possible. In other words, if either the term "AIDS" or the term "HIV",
or neither, represents conceptually independent entities but rather
purely
semantic constructs, then biologically there can be no cause-and-effect
relationship between these two terms, i.e. between the postulated
pathogen
"HIV" and the supposed definable disease entity "AIDS".
The causative factor, the "retrovirus HTLV-III"
(later termed "HIV") was introduced by Robert Gallo in 1984 (then a
retrovirologist
in the Tumour Biology Laboratory in the National Cancer Institute at
Bethesda).
On May 4, 1984 together with collaborators from his own laboratory and
other research centres and hospitals as well as workers at the
pharmaceutical
company Litton Bionetics, he published four basic papers in Science
(3-6). These supposedly described the identification, isolation and
continuous
production of a newly discovered type of retrovirus (since 1987 called
"HIV") as well as the serological analysis of this "HIV" and of tests
"capable
of detecting antibodies to HIV" in the sera of "patients with AIDS or
pre-AIDS".
The simultaneous publication of these four papers by Gallo et al was
shortly
preceded by a patent application for "HIV antibody tests" and by Reagan’s
US Health Secretary’s announcement at a press conference attended by
Robert
Gallo himself before the world’s media that Robert Gallo and his team had
"discovered the probable cause of AIDS".
The first Science paper of May 4, 1984
begins with the fundamental assumption: "epidemiological data suggest
that
the acquired immunodeficiency syndrome (AIDS) is caused by an infectious
agent that is horizontally transmitted by intimate contact or blood
products"
(3). The word ‘probably’ employed by the US minister only a few days
before
was no longer mentioned by Gallo et al.
The fourth and last Science paper of that
date ends with the conclusion: "The data presented here and in the
accompanying
reports suggest that HTLV-III is the primary cause of AIDS" (6).
(HTLV-III
= HIV). Gallo et al's conclusion proves that they did not postulate a
direct
cause-and-effect relationship between "HIV" and "AIDS", declaring "HIV"
to be only the primary cause of "AIDS": "Although the disease is
manifested by opportunistic infections, predominantly Pneumocystis
Carinii
Pneumonia, and by Kaposi's Sarcoma, the underlying disorder affects the
patient’s cell-mediated immunity, resulting in absolute lymphopenia and
reduced subpopulation of helper T lymphocytes (OKT4+)" (3). Gallo et al
by no means, therefore, postulated that "HIV" was the direct cause
of "AIDS", rather, they only claimed "HIV" is the cause of "AID" (AID =
Acquired Immuno Deficiency = reduced sub-population of T-helper
lymphocytes).
The syndrome "S" ("manifested by opportunistic infections (OI), mainly
Pneumocystis Carinii Pneumonia (= PCP), and Kaposi's Sarcoma (= KS)") was
presented by Gallo et al like commonplace as the necessary consequence
of "AID".
The scheme of Gallo et al is as follows:
1. "HIV" causes "AID" as a consequence of
the infection and sooner or later the destruction of T-helper
lymphocytes.
2. As a consequence of the decrease of cellular
immunity, the control of opportunistic pathogens and cancer cells by
T-helper
lymphocytes breaks down as a result of which, syndrome "S" develops.
The short version of Gallo et al’s plague
formula is "HIV = AID = S".
The two part causal chain "HIV causes AIDS"
actually turns out to consist of three parts, and Gallo et al’s claim
that
"HTLV-III" (= "HIV") is the primary cause of "AIDS" (6) is a fusion of
two hypothetical causal assertions, and a fictitious end-effect
assertion.
This is because Gallo et al's published data say nothing about whether
"AID" really does cause "S"; they can at most suggest a cause-and-effect
relationship between "HIV" and "AID". Whether "S" can be the result of
"AID" is for several reasons highly doubtful. "S" is somewhat
chameleon-like
due to numerous re-definitions undergone, so that the existence of "S"
as a "separate disease entity" (4), in the sense of a biological disease
entity, can no longer be rationally made out. Individual, defined
diseases,
which initially made up part of the syndrome were years later expressly
removed again. In the end a wild collection of 29 old infections and
non-infectious
diseases has been collected together to constitute the syndrome "S", of
which several are part of "S" even if the "HIV" status is negative or
indeterminate
(7).
The latter means that "AID" cannot be the
cause of "S" because "AID" is supposed to be the result of "HIV", in
order
that Gallo et al’s plague formula "HIV = AID = S" as a causal chain is
upheld, yet "AID" due to different reasons can exist independently of
"HIV".
Nothing is given whereby "AID" must be the cause of "S". "AID" and "S"
could, instead, have a common cause which need have no causal
relationship
with a hypothetical "retrovirus HIV".
The pretence of a pseudo-biological cause-and-effect
relationship expressed by the plague formula "HIV = AID = S" has made a
leading AIDS critic, who has presented the most comprehensive clinical
analysis of the AIDS phenomenon, say "AIDS, in short, has become a
schizophrenic
disease" (8).
How then, can a semantic construct of a collection
of mostly contradictory diseases be the result of a supposed biological
causal chain, which itself in turn is made up of hypothetical constructs
as cause-and-effect factors? Because the premises and conclusions (3,6)
which underlie Gallo et al’s plague formula can be falsified
convincingly.
Gallo et al have claimed that "epidemiological
data prove that an infectious agent (3) is the cause of "AID", and "AID"
is the cause of "S"." Essentially, Gallo et al arrived at this conclusion
from the findings of the CDC that "S" ("OI, mainly PCP, and KS") is
significantly
connected with very frequent promiscuity and predominantly receptive anal
intercourse in homosexual men in the metropolitan areas in the US (3).
However, this conclusion only demonstrates the arbitrary and selective
interpretation of the clinical data by the CDC and Gallo et al.
Highly promiscuous and predominantly receptive
(unprotected) anal intercourse are specifically indicators simultaneously
for infectious and non-infectious causal factors for "S" ("OI, mainly
PCP,
and KS") as well as "AID" (decline in T-helper lymphocytes in blood
serum).
The conclusion of a new infectious pathogen and simultaneous exclusion
of all non-infectious causal factors is by no means compelling, although
it determines to this day the theory that "HIV causes AIDS".
Highly promiscuous behaviour and predominant
receptive anal intercourse closely correlate with consumption of sexual
stimulants, above all amyl and isobutyl nitrites. 95% of homosexual men
in the US report regular use of nitrite (9,10). Nitrite inhalation
relaxes
the smooth anal muscles, raises blood flow to the penis, raises pain
threshold,
heightens orgasm and unleashes a mild state of intoxication in the brain.
Nitrite use predominantly but not exclusively became known in homosexual
sex partners, and has been approaching ubiquitous in surveyed homosexual
men in Western countries since the mid-70s (11,13).
High frequency promiscuity and predominantly
receptive anal intercourse very often entails concomitant increased
multi-infectivity
and provocation of administrating antimicrobials, chemotherapy,
antibiotics,
antiparasitica, antimycotica, virusstatica and corticosteroids (14). The
first report by the CDC in June 1981 of five diseased homosexual men
being
treated for PCP contains some clinical information of their medical
history
and medication, because at the time, the all-encompassing description
AIDS,
masking the real symptoms, had not yet become entrenched: The five
homosexual
patients had not had sexual relations between themselves. All of the five
patients used nitrites, and all five had been treated with TMP/SMX (TMP
= trimethoprim, SMX = sulfamethoxazole) (15).
The substance TMP/SMX, also known as bactrim
and septrin were introduced in the early 70s as a double
chemotherapeutical
folic acid inhibitor. Nitrite and SMX (a sulphonamide derivative) are
strongly
electrophilic oxidising agents. Both oxidise ferrous iron in haemoglobin
to ferric, and thereby reduce oxygen-binding capacity of red blood cells.
This causes methaemoglobulinaemia (16,20), a progressively
life-threatening
deficiency in oxygen supply into the respiration chain of the
mitochondria.
The latter are former bacteria, which, as multifunctional organelles,
supply
energy to the whole cell in form of adenosine triphosphate (ATP) produced
in oxidative phosphorylation (21). Oxygen-dependent ATP synthesis and its
resulting oxygen metabolites control the cell division cycle. If too
little
oxygen is transported to the respiratory chain, the ratio of oxidative
ATP production in the respiration chain (normally about 90%) may become
inverted in favour of the non-oxidative ATP production (normally about
10%). Latest experimental findings suggest that the redox balance
controls
the genetic expression of proteins for the enzymes of the non-oxidative
ATP production (glycolysis) (22).
Under normal physiological conditions, there
is a rhythm of phase-linked change between oxidative energy production
in the mitochondria and the change to non-oxidative glycolysis during the
late stage of cell division (the S-phase of mitosis). If, through lack
of oxygen under conditions of methaemoglobulinaemia, the genetic
expression
of glycolytic enzymes is not sufficiently inhibited (23), the cell may,
despite intact mitochondria, and the presence of residual molecular
oxygen,
switch to permanent non-oxidative glycolysis and cationic load reversal.
This results in unrestrained cell division, which may ultimately lead to
transformation to a tumour cell.
Along the oxygen transport route in the bloodstream,
conditions in the most minute capillaries with a diameter below 100
nanometres,
because of altered partial pressure of oxygen, are particularly
favourable
for the oxidation of the red haemoglobin, which can only bind oxygen when
being in reduced form. Through diffusion and association to essential
fatty
acids through transit routes of the basic-tissues it can deliver oxygen
to individual cells. The mechanism of unrestrained activation of cell
division
(hyperplasia) in methaemoglobulinaemia, may, therefore, following
hypoxaemic
stress, above all in the smallest capillaries, affect the cells of the
walls, – the endothelial cells. These endothelial cells are in direct
contact
with the hypoxaemic red blood cells. If hyperplastic conversion of
endothelial
cells occurs, that is called Kaposi's Sarcoma. On the other hand,
especially
in rapidly dividing cells such as in thymus-matured precursor cells of
T-helper lymphocytes, ATP production can decline to a critical value, if
oxygen turnover is reduced permanently even by a small amount. This is
a control mechanism, which in turn may affect the rate of mitosis. This
interaction of haemoglobin oxidation by nitrites and antimicrobial drugs
with oxidative phosphorylation may, in a situation of increased
simultaneous
consumption of T-helper lymphocytes as a result of slowing maturation of
T-helper lymphocytes, be in part a cause of "AID".
*This chain of causal events is also
supported by the "frightening possibility" (24) that nitrites may turn
most classes of antibiotics into carcinogens (25). Excessive antibiotic
consumption (whether prescribed or not; in a study 40% of male
homosexuals
admitted preventive use (26)) in conjunction with nitrites is a
frequently
encountered pattern of behaviour among male homosexuals especially in the
large urban areas in Western countries (27).
Hypoxaemic stress can, therefore, explain
the contradiction of simultaneous appearance of malignant hyperplasias
(KS, lymphomas) and opportunistic infections, mainly PCP, in homosexual
men (approx. 2/3 of "AIDS cases" in Western countries, excluding covered
homosexual "AIDS patients" estimated by orthodox "AIDS"-doctors to amount
to 50% of so-called heterosexual risk groups (28)), without ever
introducing
a hypothetical "retroviral" cause to explain the pathophysiology.
In contrast to this clear finding, Gallo et
al tried to resolve the clinical contradiction between OI and KS by
constructing
a new "retrovirus HIV". Gallo et al’s so-called retroviruses "HTLV-I" and
"HTLV-II" are said to cause rare forms of leukaemia, i.e. cancers of the
white blood cells, whereas "HTLV-III" (="HIV") is said to kill T-helper
lymphocytes.
This concept has completely failed. The cytopathic
effects of "HIV" demonstrated by Gallo et al have turned out to be
laboratory
artefacts (29). Gallo et al’s claim that "HIV" kills T-helper lymphocytes
could, despite changing the theories, not be confirmed (30-33).
The disease theory "HIV causes AIDS" is itself
based on several serious clinical misconceptions:
1. The agent causing PCP is not as Gallo
claimed a protozoon. The aetiology according to which after the
destruction
of T-helper lymphocytes by "HIV-infection", Carinii pneumocytes, the
cause
of PCP, could escape control by T-helper lymphocytes and multiply
unrestrictedly,
is objectively wrong. Such protozoa simply do not exist (34,35). What is
involved are micro-fungi that are inhaled in the air, and which, for
example,
in the case of increased cell decay following hypoxaemic metabolic
changes
(including "AIDS" without "HIV"), find fertile terrain in the alveoli of
the lungs. In this way, a harmless fungus (saprophyte) becomes the
dangerous
cause of PCP.
2. Contrary to what Gallo et al claimed, T-helper
lymphocytes do not suppress the growth of cancer cells, because cancer
cells do not have antigens through which T-helper lymphocytes could
identify
them (36). This means that the hypothetical destruction of T-helper
lymphocytes
by "HIV" and the ensuing disappearance of the suppression of KS cells
cannot
be the cause of KS. The predicted increase of all other types of
carcinoma
in "AIDS patients" resulting from the disappearance of the surveillance
of cancer cells after the postulated destruction of T-helper lymphocytes
by "HIV-infection" did not occur (37).
3. Contrary to the assumption of the CDC and
Gallo, the hypothetical "HIV infection" of T-helper lymphocytes despite
the postulated essentially alarm function of T-helper lymphocytes also
for antibody production by B-plasma cells did not result in destroying
defence capacity against all microbes. Unlike patients with
impaired immune functions, E.G. intensive care patients in whom mortality
following typical bacterial infections is up to 80%, strikingly in the
"immune deficiency syndrome AIDS", bacterial infections are rarely seen.
The CDC under the category "AIDS indicator diseases" states explicitly
for "bacterial infections, frequent or repeated": "not applicable as
indicator
of AIDS in adults/adolescents" (37).
4. A fundamental pillar of the disease theory
of Gallo et al according to which "HIV causes AIDS", is severely dented
by the actual epidemiological situation over the 15 years 1982-1997. For
example, in 1997 the German "AIDS Centre" registered 2736 KS cases in
total
with 2505 KS cases in the category "homosexuals". The remaining KS cases
were in "heterosexual risk groups" or "no information on risk group". On
average, therefore, there were 15 KS cases a year, which were not
primarily
classified as "homosexual". Because homosexual intravenous drug users are
classified as intravenous drug users and at least 50% of the patients
classified
as "heterosexual men" and "not known" were subsequently reclassified as
homosexuals (28,38), this is of the order of magnitude to be expected for
KS cases classified as "non-homosexual men". Corresponding
epidemiological
data for the prevalence of KS are available for other Western countries
(39).
Gallo et al’s formulation "HIV = AID = S"
is not, therefore, found to be true. "AID" (measurable decline in
lymphocyte
population in the blood, especially T-helper lymphocytes) though it can
occur, in all members of "high-risk groups", is evidently not the cause
of "S" ("OI, mainly PCP, and KS") because "S" can, first, occur without
"AID" (29), and secondly, the combination of "S" (with KS) should, if the
theory were correct, not exclusively be limited to homosexual patients.
If, therefore, "S" is not necessarily the result of "AID", what then is
the common pathogenic indicator of "AID" patients as defined by Gallo et
al to be "high-risk groups" (4)?
The common factor of "AID" patients (without
necessarily resulting in "S") is obviously the unusually high uptake of
strongly oxidising substances (mitogens), and the huge variety of
exogenous
extraneous cells such as red blood cells, activated lymphocytes or sperm
cells from individuals (allogenic stimulation (29,40)). It is beyond
doubt
that this oxidative stress (i.e. pro-oxidative vs. anti-oxidative
metabolism)
of "high-risk groups", can overload the detoxification capacity and waste
disposal capacity of the body which is furthermore supported by the
finding
that asymptomatic "HIV positives" belonging to "high-risk groups" show
a strong shift from reduced to oxidised glutathione (41).
The glutathione system is essential for the
removal of oxygen free-radicals, especially in the mitochondria (42,43).
The oxidation of the central molecule of glutathione, cysteine, to
cystine,
in a chain reaction reduces the build up of glutathione and accelerates
the destruction. It follows that the systemic decline of glutathione
concentration
in HIV positives can be due to both reasons, because of decreased
synthesis
and increased disposal.
"The oxidative stress to which AIDS patients
are subjected would lead to cellular anomalies in many cells, including
lymphocytes, resulting in opportunistic infection, immunological
abnormalities
and neoplasia" (44).
Does this finding of the overload of redox
potentials in members of "high-risk groups" mean that "HIV", too, or
rather
the "anti-HIV antibodies" are the result of oxidative bombardment on the
cell-mediated immunity of the "high-risk groups"?
A specific load value of the diminution of
the reduction force in the body of members of "high-risk groups" is
hepatitis
type B, in particular, in the chronically active form (45).
Gallo et al postulated in the first paragraph
of the first publications in Science of May 4 1984 (except for the first
rebutted premise: "Epidemiological data suggest that the acquired
immunodeficiency
syndrome (AIDS) is caused by an infectious agent" and the second
(rebutted)
premise: "AID" necessarily leads to "S"), a third premise: "Although
patients
with AIDS or pre-AIDS are often chronically infected with cytomegalo
virus
or hepatitis B virus, for various reasons these appear to be
opportunistic
or coincidental infections" (3).
This claim stands the clinical history completely
on its head. "High-risk groups", in Gallo’s definition "homosexual men
with multiple sex partners, intravenous drug missusers, haemophiliacs,
blood transfusion recipients and close heterosexual contacts of members
of these high-risk groups" (6) were long before the so-called ‘sudden’
arrival of "HIV" (1978), recognised to be the most severely hepatitis-B
affected groups of patients (46-50).
Hepatitis inducers (nowadays thought to be
hepatitis-B, hepatitis-C) "appear to be thousands of times as infectious
in clinical settings as HIV and represents a much more prevalent medical
problem" (51). Hepatitis-B due to various patho-physiological reasons,
especially in the chronically active form contributes significantly to
oxidative stress, by restricting waste disposal and detoxification, and
overloading of redox potentials. The body tries to compensate for this
by increasing cortisol production. When this ultimately fails,
hypercorticolism
persists in a damaging way. A hypercatabolic metabolism results from this
(i.e. excess cell decay vs. build up) (52). Cortisol as "synergiser" for
a number of hormones and mediators effects activation of cyclic adenosine
monophosphate (cAMP) and a displacement of the cAMP/cGMP ratio as
principal
indicator for increased cell turnover (53). The net effect is a dampening
of cellular immunity and activation of humoral immunity. Resulting from
the increased cell turnover, the decreased disposal of cell debris
(because
of the dampened cellular immunity, "AID") and the strengthened autoimmune
activity, a significantly increased formation of autoantibodies occurs
which above all specifically bind to cytoskeletal proteins and
extra-cellular
proteins of the cell matrix as antigens (54, 33).
Concluding, it is fair to assume that Gallo
et al took these attributes (25) of "high-risk groups" into
consideration,
namely,
1. the excessive oxidative (mitogenic) stress
2. allogenic stimulation by foreign cell
components
3. the sharply increased antigen auto-antibody
load together with suppression of T-cell dependent immunity brought about
by synergistic effects of persistent corticolism with resulting change
in cAMP/cGMP ratio.
In their original paper ("Detection, isolation
and continuos production .." (3)), Gallo et al were only able to cite
indirect
phenomena, such as reverse transcription, ultra-thin layer electron
micrographs,
banding of protein mixtures at given densities, which according to the
established rules of virology are not acceptable as evidence for the
existence
of a virus or less a "retrovirus", because these indirect phenomena can
also be obtained in the absence of any viral entity under certain cell
culture conditions (55-60,33).
Then the question becomes increasingly pressing:
how did Gallo et al manage to produce a protein mixture in cell cultures
and in the test tube, which as the substrate in the "AIDS-test" when in
contact with serum of people in "high-risk groups", resulted in a given
rate of antigen antibody-reaction for single proteins (6)?
Gallo's papers, though written in highly technical
language do not reveal this secret of test-constructing. Only in 1987
when
the disease theory "HIV causes AIDS" led to the introduction of a highly
toxic DNA chain terminator (azidothymidine = AZT = Retrovir), was some
light shed on this matter when two of Gallo’s former collaborators and
co-authors of the original publications in Science of May 4 1984
(3-6) revealed the essential details. Mangalasseril Sarngadharan and
Phillip
Markham (collaborators of Litton Bionetics, Kensington MD, USA) published
the biochemical methods used by Gallo et al whereby they manipulated the
protein mixture, which due to self-defined conventions are said to be
"HIV
antigens" (59).
To start with, Gallo et al biochemically prepared
cell components obtained from members of "high-risk groups" according to
the self-defined rules of "retrovirus production". This procedure only
"from time to time" and only transiently (61) led to the production of
unspecific phenomena as surrogates for the existence of a new
"retrovirus".
Then they mixed lymphocytes from patients in "high-risk groups" with
exceptionally
rapidly dividing leukaemia cells (3,4). This cell mixture was then
subjected
to the effects of certain biochemical substances. They go on to say that
"in vitro stimulation was achieved by mitogens or added cells (allogenic
antigens ) ... Certain manipulation of culture conditions improved the
result, for example, co-cultivation of patients’ cells with peripheral
white blood cells, which were stimulated by mitogens, from non-infected
donors.
The "virus isolation" of cultured cells was
also significantly facilitated by adding hydrocortisone to the culture
medium" (61).
Knowing the specific antigen auto-antibody
status of "high-risk groups" patients, it is possible, therefore, to
trigger,
on demand, an antigen mixture appropriate to the auto-antibody repertoire
in serum from high-risk patients, in cell cultures of human lymphocytes,
co-cultured with leukaemic cells when subjected to specific biochemical
manipulation.

DID DR. GALLO AND HIS COLLEAGUES MANIPULATE THE "AIDS-TEST" TO ORDER?


Extract

"The hunt for the virus" 1 has degenerated into "clean torture with fatal
result" 2

By Heinrich Kremer

Continuum Summer 1998


Who, for given reasons given below casts doubt
on the theory that "HIV causes AIDS", is often confronted with the
question,
if it did not, how is it that a patient who has been diagnosed as "HIV
positive" by the test sooner or later goes on to develop AIDS? To which
the AIDS sceptic usually replies that a "HIV-positive" laboratory result,
an arbitrary defined characteristic is part of the clinical diagnosis
"AIDS".

This exchange does not advance the argument
very much as to whether "AIDS" and "HIV" are scientifically-speaking
biological
entities and if between them a biological cause-effect relationship is
possible. In other words, if either the term "AIDS" or the term "HIV",
or neither, represents conceptually independent entities but rather
purely
semantic constructs, then biologically there can be no cause-and-effect
relationship between these two terms, i.e. between the postulated
pathogen
"HIV" and the supposed definable disease entity "AIDS".

The causative factor, the "retrovirus HTLV-III"
(later termed "HIV") was introduced by Robert Gallo in 1984 (then a
retrovirologist
in the Tumour Biology Laboratory in the National Cancer Institute at
Bethesda).
On May 4, 1984 together with collaborators from his own laboratory and
other research centres and hospitals as well as workers at the
pharmaceutical
company Litton Bionetics, he published four basic papers in Science
(3-6). These supposedly described the identification, isolation and
continuous
production of a newly discovered type of retrovirus (since 1987 called
"HIV") as well as the serological analysis of this "HIV" and of tests
"capable
of detecting antibodies to HIV" in the sera of "patients with AIDS or
pre-AIDS".
The simultaneous publication of these four papers by Gallo et al was
shortly
preceded by a patent application for "HIV antibody tests" and by Reagan’s
US Health Secretary’s announcement at a press conference attended by
Robert
Gallo himself before the world’s media that Robert Gallo and his team had
"discovered the probable cause of AIDS".

The first Science paper of May 4, 1984
begins with the fundamental assumption: "epidemiological data suggest
that
the acquired immunodeficiency syndrome (AIDS) is caused by an infectious
agent that is horizontally transmitted by intimate contact or blood
products"
(3). The word ‘probably’ employed by the US minister only a few days
before
was no longer mentioned by Gallo et al.

The fourth and last Science paper of that
date ends with the conclusion: "The data presented here and in the
accompanying
reports suggest that HTLV-III is the primary cause of AIDS" (6).
(HTLV-III
= HIV). Gallo et al's conclusion proves that they did not postulate a
direct
cause-and-effect relationship between "HIV" and "AIDS", declaring "HIV"
to be only the primary cause of "AIDS": "Although the disease is
manifested by opportunistic infections, predominantly Pneumocystis
Carinii
Pneumonia, and by Kaposi's Sarcoma, the underlying disorder affects the
patient’s cell-mediated immunity, resulting in absolute lymphopenia and
reduced subpopulation of helper T lymphocytes (OKT4+)" (3). Gallo et al
by no means, therefore, postulated that "HIV" was the direct cause
of "AIDS", rather, they only claimed "HIV" is the cause of "AID" (AID =
Acquired Immuno Deficiency = reduced sub-population of T-helper
lymphocytes).
The syndrome "S" ("manifested by opportunistic infections (OI), mainly
Pneumocystis Carinii Pneumonia (= PCP), and Kaposi's Sarcoma (= KS)") was
presented by Gallo et al like commonplace as the necessary consequence
of "AID".

The scheme of Gallo et al is as follows:

1. "HIV" causes "AID" as a consequence of
the infection and sooner or later the destruction of T-helper
lymphocytes.

2. As a consequence of the decrease of cellular
immunity, the control of opportunistic pathogens and cancer cells by
T-helper
lymphocytes breaks down as a result of which, syndrome "S" develops.

The short version of Gallo et al’s plague
formula is "HIV = AID = S".

The two part causal chain "HIV causes AIDS"
actually turns out to consist of three parts, and Gallo et al’s claim
that
"HTLV-III" (= "HIV") is the primary cause of "AIDS" (6) is a fusion of
two hypothetical causal assertions, and a fictitious end-effect
assertion.
This is because Gallo et al's published data say nothing about whether
"AID" really does cause "S"; they can at most suggest a cause-and-effect
relationship between "HIV" and "AID". Whether "S" can be the result of
"AID" is for several reasons highly doubtful. "S" is somewhat
chameleon-like
due to numerous re-definitions undergone, so that the existence of "S"
as a "separate disease entity" (4), in the sense of a biological disease
entity, can no longer be rationally made out. Individual, defined
diseases,
which initially made up part of the syndrome were years later expressly
removed again. In the end a wild collection of 29 old infections and
non-infectious
diseases has been collected together to constitute the syndrome "S", of
which several are part of "S" even if the "HIV" status is negative or
indeterminate
(7).

The latter means that "AID" cannot be the
cause of "S" because "AID" is supposed to be the result of "HIV", in
order
that Gallo et al’s plague formula "HIV = AID = S" as a causal chain is
upheld, yet "AID" due to different reasons can exist independently of
"HIV".
Nothing is given whereby "AID" must be the cause of "S". "AID" and "S"
could, instead, have a common cause which need have no causal
relationship
with a hypothetical "retrovirus HIV".

The pretence of a pseudo-biological cause-and-effect
relationship expressed by the plague formula "HIV = AID = S" has made a
leading AIDS critic, who has presented the most comprehensive clinical
analysis of the AIDS phenomenon, say "AIDS, in short, has become a
schizophrenic
disease" (8).

How then, can a semantic construct of a collection
of mostly contradictory diseases be the result of a supposed biological
causal chain, which itself in turn is made up of hypothetical constructs
as cause-and-effect factors? Because the premises and conclusions (3,6)
which underlie Gallo et al’s plague formula can be falsified
convincingly.

Gallo et al have claimed that "epidemiological
data prove that an infectious agent (3) is the cause of "AID", and "AID"
is the cause of "S"." Essentially, Gallo et al arrived at this conclusion
from the findings of the CDC that "S" ("OI, mainly PCP, and KS") is
significantly
connected with very frequent promiscuity and predominantly receptive anal
intercourse in homosexual men in the metropolitan areas in the US (3).
However, this conclusion only demonstrates the arbitrary and selective
interpretation of the clinical data by the CDC and Gallo et al.

Highly promiscuous and predominantly receptive
(unprotected) anal intercourse are specifically indicators simultaneously
for infectious and non-infectious causal factors for "S" ("OI, mainly
PCP,
and KS") as well as "AID" (decline in T-helper lymphocytes in blood
serum).
The conclusion of a new infectious pathogen and simultaneous exclusion
of all non-infectious causal factors is by no means compelling, although
it determines to this day the theory that "HIV causes AIDS".

Highly promiscuous behaviour and predominant
receptive anal intercourse closely correlate with consumption of sexual
stimulants, above all amyl and isobutyl nitrites. 95% of homosexual men
in the US report regular use of nitrite (9,10). Nitrite inhalation
relaxes
the smooth anal muscles, raises blood flow to the penis, raises pain
threshold,
heightens orgasm and unleashes a mild state of intoxication in the brain.
Nitrite use predominantly but not exclusively became known in homosexual
sex partners, and has been approaching ubiquitous in surveyed homosexual
men in Western countries since the mid-70s (11,13).

High frequency promiscuity and predominantly
receptive anal intercourse very often entails concomitant increased
multi-infectivity
and provocation of administrating antimicrobials, chemotherapy,
antibiotics,
antiparasitica, antimycotica, virusstatica and corticosteroids (14). The
first report by the CDC in June 1981 of five diseased homosexual men
being
treated for PCP contains some clinical information of their medical
history
and medication, because at the time, the all-encompassing description
AIDS,
masking the real symptoms, had not yet become entrenched: The five
homosexual
patients had not had sexual relations between themselves. All of the five
patients used nitrites, and all five had been treated with TMP/SMX (TMP
= trimethoprim, SMX = sulfamethoxazole) (15).

The substance TMP/SMX, also known as bactrim
and septrin were introduced in the early 70s as a double
chemotherapeutical
folic acid inhibitor. Nitrite and SMX (a sulphonamide derivative) are
strongly
electrophilic oxidising agents. Both oxidise ferrous iron in haemoglobin
to ferric, and thereby reduce oxygen-binding capacity of red blood cells.
This causes methaemoglobulinaemia (16,20), a progressively
life-threatening
deficiency in oxygen supply into the respiration chain of the
mitochondria.
The latter are former bacteria, which, as multifunctional organelles,
supply
energy to the whole cell in form of adenosine triphosphate (ATP) produced
in oxidative phosphorylation (21). Oxygen-dependent ATP synthesis and its
resulting oxygen metabolites control the cell division cycle. If too
little
oxygen is transported to the respiratory chain, the ratio of oxidative
ATP production in the respiration chain (normally about 90%) may become
inverted in favour of the non-oxidative ATP production (normally about
10%). Latest experimental findings suggest that the redox balance
controls
the genetic expression of proteins for the enzymes of the non-oxidative
ATP production (glycolysis) (22).

Under normal physiological conditions, there
is a rhythm of phase-linked change between oxidative energy production
in the mitochondria and the change to non-oxidative glycolysis during the
late stage of cell division (the S-phase of mitosis). If, through lack
of oxygen under conditions of methaemoglobulinaemia, the genetic
expression
of glycolytic enzymes is not sufficiently inhibited (23), the cell may,
despite intact mitochondria, and the presence of residual molecular
oxygen,
switch to permanent non-oxidative glycolysis and cationic load reversal.
This results in unrestrained cell division, which may ultimately lead to
transformation to a tumour cell.

Along the oxygen transport route in the bloodstream,
conditions in the most minute capillaries with a diameter below 100
nanometres,
because of altered partial pressure of oxygen, are particularly
favourable
for the oxidation of the red haemoglobin, which can only bind oxygen when
being in reduced form. Through diffusion and association to essential
fatty
acids through transit routes of the basic-tissues it can deliver oxygen
to individual cells. The mechanism of unrestrained activation of cell
division
(hyperplasia) in methaemoglobulinaemia, may, therefore, following
hypoxaemic
stress, above all in the smallest capillaries, affect the cells of the
walls, – the endothelial cells. These endothelial cells are in direct
contact
with the hypoxaemic red blood cells. If hyperplastic conversion of
endothelial
cells occurs, that is called Kaposi's Sarcoma. On the other hand,
especially
in rapidly dividing cells such as in thymus-matured precursor cells of
T-helper lymphocytes, ATP production can decline to a critical value, if
oxygen turnover is reduced permanently even by a small amount. This is
a control mechanism, which in turn may affect the rate of mitosis. This
interaction of haemoglobin oxidation by nitrites and antimicrobial drugs
with oxidative phosphorylation may, in a situation of increased
simultaneous
consumption of T-helper lymphocytes as a result of slowing maturation of
T-helper lymphocytes, be in part a cause of "AID".

*This chain of causal events is also
supported by the "frightening possibility" (24) that nitrites may turn
most classes of antibiotics into carcinogens (25). Excessive antibiotic
consumption (whether prescribed or not; in a study 40% of male
homosexuals
admitted preventive use (26)) in conjunction with nitrites is a
frequently
encountered pattern of behaviour among male homosexuals especially in the
large urban areas in Western countries (27).

Hypoxaemic stress can, therefore, explain
the contradiction of simultaneous appearance of malignant hyperplasias
(KS, lymphomas) and opportunistic infections, mainly PCP, in homosexual
men (approx. 2/3 of "AIDS cases" in Western countries, excluding covered
homosexual "AIDS patients" estimated by orthodox "AIDS"-doctors to amount
to 50% of so-called heterosexual risk groups (28)), without ever
introducing
a hypothetical "retroviral" cause to explain the pathophysiology.

In contrast to this clear finding, Gallo et
al tried to resolve the clinical contradiction between OI and KS by
constructing
a new "retrovirus HIV". Gallo et al’s so-called retroviruses "HTLV-I" and
"HTLV-II" are said to cause rare forms of leukaemia, i.e. cancers of the
white blood cells, whereas "HTLV-III" (="HIV") is said to kill T-helper
lymphocytes.