15 YEARS OF AIDS
The continuous failure in the prevention and
treatment of AIDS is rooted in the misinterpretation of an inflammatory
auto immune process as a lethal, viral venereal disease
By A. Hässig, H. Kremer, S. Lanka, W-X Liang, K. Stampfli
Summary - The question of the specificity of the anti-HIV antibody test has to be re-evaluated as it was shown that the viral enrichment obtained from
co-cultivations of patients lymphocytes with fetal cord blood by BARRÉ-SINOUSSI
et al. and leukaemia cells by GALLO et al., exclusively consisted of proteins
of the cell types used in the cell culture. This precludes a clear separation
of presumed retroviral and cellular proteins or extracellular matrix proteins.
In this context it was shown that the anti-HIV antibody test detects autoimmune
antibodies directed against cyto-skeletal proteins e.g. the liver cells.
Strongly augmented anti-actin autoantibodies is considered close to pathognomonic
for chronically active hepatitis. The original assumption that "reverse
transcription" from RNA to DNA is evidence for the existence of retroviruses,
was wrong. In fact, "reverse transcription" is a vital mechanism
for the maintenance the genome. The decrease in numbers of circulating
CD4 lymphocytes can be explained by a stress-induced hyper-cortisolism.
Up to date, direct HIV-mediated destruction of CD4 lymphocytes could not
be proved. The same is true for measuring of the "viral load".
Shortcomings of the applied method to quantify the "viral load"
do not permit definitive conclusions. Possibly, it may be taken as an expression
of a stress-induced weakening of the cellular immune reactions, in the
course of which the nucleoside fragments resulting from the current cell
turnover are inadequately eliminated. Furthermore, the treatment of patients
with nucleoside analogues has a toxic effect on both the genome of the
cell-nucleus and the mitochondria. The latter, therefore, may produce insufficient
amounts of ATP, causing organ failure and, eventually, death. The synthetic
protease inhibitors used these days are associated with serious side-effects.
Therefore, it seems worthwhile, in these patients, to bring back the catabolic
situation due to whole body inflammation to homeostasis by administering
anabolic phyto-polyphenolic compounds.
AIDS is the abbrevation for acquired immunodeficiency syndrome. AIDS,
as a term for an illness, originated in the search by the American Centers
of Disease Control for sick homosexual men, also suffering from Kaposi's
Sarcoma (KS) and/or Pneumocystis carinii pneumonia (PCP). In 1983 BARRÉ-SINOUSSI
et al. reported on a T-lymphotropic retrovirus which they allegedly isolated
from an enlarged lymphnode of a homosexual patient (1). In 1984 GALLO et
al. reported the alleged isolation of an identical retrovirus from CD4-lymph
cells from homosexual patients, clinically diagnosed as suffering from
AIDS (2). BARRÉ-SINOUSSI et al. co-cultivated these patients lymph
cells in question with fetal cord blood, and GALLO et al. co-cultivated
theirs with leukaemia cells. Initially, these laboratory methods must raise
doubts as to whether the isolation of a new human retrovirus is evident
just by these data. GALLO et al. stated that their allegedly isolated retrovirus
caused the destruction of CD4 lymphocytes in those patients, whose heterogenic
illness was taken as an after-effect of the CD4-cell destruction and so
subsumed as AIDS. Besides, GALLO et al. announced that in due time a vaccine
would be available for the formation of antibodies against the discovered
virus (2). Today, fifteen years later, the question still remains open,
whether HI retroviruses actually do exist or whether the postulated retroviral
HIV-antigens as well as the postulated HIV reverse transcription are a
matter of human protein molecules derived from cells in co-cultured cell
cultures used by both BARRÉ-SINOUSSI et al. and GALLO et al.. The
most extensive investigations in this regard are owed to ELENI PAPADOPULOS-ELEOPULOS
and her group in Perth, Australia. In 1993 they published a review concluding
that there is no evidence for the existence of HI viruses (3). In 1994
LANKA demonstrated that all retroviruses, including HIV, are biologically
inexistent and their phenomenology is based on laboratory artefacts (4-6).
ELENI PAPADOPULOS confirmed LANKA’s interpretation in a recent comprehensive
These fundamental counter-statements to the current HIV-AIDS-theory
have been strongly supported in the last few years. Upon investigations
in order to develop a vaccine against HIV it became apparent, that the
enrichment of presumed HIV-1 preparations, considered as pure, consist
of proteins of the cell types used in the cell cultures, which resist a
clean separation into presumed retroviral and cellular proteins, i.e. extracellular
matrix proteins. Above all, these cell proteins, also occur in the inside
of extracellular particles, which have been misread as it seems as so-called
HI virions by the retrovirologists (8-10). These findings were to be expected
as GALLO et al., when developing the AIDS test, did not investigate the
presence of cells own proteins in the protein mixture, released during
the co-cultivation of patients lymphocytes and leukaemia cells. Upon developing
the ELISA- and Western Blot tests it should have been imperative to consider
proteins released from stimulated leukaemia cells, not being mixed with
patients lymphocytes, and to differentiate these from the ones, released
only after addition of patients lymphocytes.
In view of this it seems to be mandatory to re-evaluate the question
of the specificity of the anti-HIV-antibody test.
What is the laboratory finding "anti-HIV-positive" based
In a series of preceding reports we have discussed this question in
detail (11-14). We came to the conclusion: the laboratory finding "anti-HIV-positive"
is primarily the expression of an autoimmune activation of the immune system
linked to a persistant catabolic state of metabolism. In view of the fact
that the diseases grouped under the term AIDS are limited to risk groups
such as homosexuals, drug addicts and recipients of blood products contaminated
with parenterally transmitted hepatitis inductors, the question is raised,
whether the anti-HIV test determines autoantibodies directed against cell
envelope structures with a specificity to the body's own proteins of the
host cells. It has been known for over twenty years that chronically active
hepatitis (currently hepatitis B, hepatitis C and autoimmune hepatitis
without evident antiviral antibodies) react by the formation of autoimmune
antibodies directed against cyto-skeletal proteins of the liver cells.
Thus, the raised anti-actin-autoantibodies are pathognomonic for chronically
active hepatitides (15). JOHNSON et al., in 1965, were the first
to report on anti-actin-autoantibodies (16). They described autoantibodies
directed against smooth muscle cells and showed that this had to be considered
as characteristic indication of "lupoid hepatitis". In 1973 GABBIANI
et al. demonstrated that autoantibodies directed against smooth muscle
cells react with actin-containing microfilaments (17). Further investigations
indicate that autoantibodies with anti-actin specificity are to be classified
within the big group of autoantibodies against filamentous proteins of
smooth muscle fibres. 3 - 18% of healthy individuals present low titer
autoantibodies against cyto-skeletal proteins (18). High titer anti-actin
autoantibodies, on the other hand, are only found in patients suffering
from chronically active hepatitis and/or biliary cirrhosis (19). In 1994
BERMAS et al. showed that both sera from patients with lupus erythematosus
and from mice suffering from the same illness react with glycoprotein 120
and peptides of the postulated HIV-1 envelope (20). They further proved
that control sera of healthy individuals and patients with other autoimmune
diseases contain small amounts of the same autoantibodies. Last but not
least, they showed that autoantibodies reacting with glycoprotein 120 do
not possess antinuclear specificity. They refrained from investigating
a specificity against cytoskeletal proteins of these autoantibodies.
Evidence is given that the anti HIV test does not indicate antibody
formation against the postulated retroviruses as, during the last decade
in Germany, not a single seroconversion has been observed in inprisoned
drug addicts. All sero-positive drug addicts acquired their anti HIV "positivity"
before their imprisonement. In opposition to this, seroconversion by hepatitis
B inductors was recorded in intravenous drug addicts (21-23). The same
was also observed in haemophiliacs, i.e. despite continuous substitution
with hepatitis-contaminated blood products approx. a third of these individuals
never become anti-HIV positive. This is characteristic for the individual
response to autoimmune reactions against cyto-skeletal proteins in the
host cells, in which GIRARD and SEN?CAL observed a polyreactivity (24).
The individual autoimmune reactivity either appears at first contact or
fails to appear even at multiple contacts.
We conclude that a positive anti-HIV test does not indicate an antibody
formation against "retroviral HIV antigens". Low titer "anti
HIV" antibodies are common even in healthy individuals. High titer
"anti HIV" antibodies are pathognomonic in chronically active
hepatitis. The anti HIV test does not answer the question whether anti
HIV antibodies occur or not; the test differentiates between "plenty
= positive" and "few = negative".
Rethinking as to "Reverse transcription"
The error, taking proteins resulting from "HIV" isolation
for retroviral proteins, dates back to 1970. The paradigm, that DNA codes
information and programs relating to all physiological and phenomenological
aspects of all organisms, resulted in the postulation of the irreversibility
of the genetic flow of information for the synthesis of proteins - from
DNA via messenger substance (RNA) to proteins. This was the crucial genetic
dogma (25). Despite the proven reversibility in 1970, that from RNA DNA
can remerge, this fact was postulated as an exception that proves the rule
by stating the existence of retroviruses, qualified for this reversibility,
which, at this time, were only considered as tumour viruses (26, 27).
With the discovery of this enzymatic activity in all living cells it
soon became clear that the evidence of the function of "reverse transcription"
from DNA into RNA was not a proof for the existence of retroviruses, because
the genome of all eukaryotic cells is clearly marked by this activity (28,
29). Retrospectively, it seems rather astonishing that in 1983 MONTAGNIER
and in 1984 GALLO still postulated a new retrovirus despite the fact that
a new viral entity had never been isolated or described, according to the
standard regulations in virology. As a matter of fact, the enzyme Reverse
Transcriptase from ÒHIVÒ has never been isolated or described,
but only inferred from functions to its existence, when new formation from
DNA into RNA was proven by laboratory techniques.
Since 1985 it has been known that the "Reverse Transcription"
plays a decisive role in the maintenance of the structure of the genome,
by repairing chromosome fractures and, especially, by limiting
the loss of chromosomal end components, the telomeres occurring at cell
replication (30-33). The respective enzymes for this kind of reverse transcription,
the telomerases dispose of a type-specific RNA matrix for the formation
of the repeating telomer units. Somatic human cells, that do not belong
to the reproductive path, cannot adapt to the shrinking of their telomeres
when replicating and so cease the replication at a certain degree of depletion.
Up to date, the influence of nucleoside analgues on the action of telomeres
at replication has obviously not been investigated. We could trace only
two publications, in 1996, which describe an in vitro investigation of
nucleoside analogues inhibiting the telomerase activity. In our view, the
knowledge, already gained in 1980, on the vital physiological function
of "reverse transcription", should have lead to a rethinking
as to the establishing of nucleoside analogues as pharmacological inhibitors
of the "Reverse Transcription" of the postulated HI viruses and,
according to knowledge of that time on the physiological function of the
"Reverse Transcription", it should have been rejected (34,35).
What is the decrease of CD4-lymphocytes in AIDS based on?
The decrease of the circulating CD4-lymphocytes in the blood stream
during progressive immune deficiency in AIDS has generally been explained
by the progressive destruction caused by HI viruses (36). Four years ago
CARBONARI et al. showed in an in vitro investigation that the apoptosis
of the lymphocytes in AIDS patients is mainly related to CD8 - T-cells
and CD19 B-cells (37). FINKEL et al. then pointed out that apoptosis concerns
mainly "bystander" cells and spares supposedly infected cells
from so-called HIV- and SIV-lymphnodes (38). These reports remind us of
FAUCI's classical publications of the 70's in which he and his working
group clearly demonstrated that, in persisting hypercortisolism, an increasing
number of CD4-cells leave the blood stream and can thus activate B-cells
in the marrow (39-44). The "migrated" CD4-cells return to the
blood stream upon dropping to normal values of the cortisol level.
At the beginning of 1995 WEI and HO et al. published a report in which
they declared, that the extremely fast multiplication of HI-1 viruses produces
a raised turnover of CD4-lymphocytes (45, 46). Towards the end of 1996
WOLTHERS et al. showed that the telomere length of CD4-lymphocytes in anti-
HIV positive individuals remains normal, whereas the one of CD8-cells decreases
During the latest international congress of leading HIV scientists the
long-term criticism of the HIV/AIDS theory has been confirmed: despite
intense and precise investigations there was no proof of a pathophysiological
mechanism explaining the different reaction of CD4- and CD8- lymphocytes
to the postulated retrovirus HIV (48). It was literally stated: "The
riddle of CD4 cell loss remains unresolved." Paul Johnson of the Harvard
Medical School in Boston voiced in a disillusioned way the helplessness
of the conventional AIDS scientists: "We are still very confused about
the mechanism that leads to CD4 depletion; but at least now we are confused
at a higher level of understanding." In other words, FAUCI's
pioneering work, based in the seventies, on experimental traumatology fell
into oblivion. CALVANO clearly documented in a review published in 1986
that the selective depletion of CD4-lymphocytes is induced by neuroendocrine
mechanisms in traumatic conditions such as injuries and burns, whereas
its proportions depend on the degree of hypercortisolism (49). It remains
enigmatic why FAUCI, after having joined the AIDS research, never again
mentioned his own reports.
What does the "viral load" measure?
Immediately, after the publication of WEI's and HO's reports in January
1995 (45,46) in which they put forward the hypothesis that HI viruses multiply
at raving speed destroying a similar number of CD4 helper cells, quantitative
tests based on the genetic multiplication method PCR were introduced and
so a large number of HIV in the blood stream was postulated. It has been
well known among HIV scientists that the so-called viral load, i.e. the
measurement of the "viral load" is no evidence of the entire
virus genome or intact viruses (50). The "viral load" measures
short components of the messenger substance RNA, attributed to the HI viruses.
Because the HI virus genome per se never could be described it is impossible
to designate these RNA fragments as viral. Going through the records of
the presumed characterisation of HIV it can be inferred that all components
- proteins and genetic substance - attributed to “HIV”, are of pure cellular
origin (3-7). Therefore, the results of the "viral load" can
only have an indirect significance, such as the measurement of an increase
or decrease of cellular RNA, as it can be observed as increasing in catabolic
conditions of cell disintegration and decreasing in anabolic conditions.
However, these results cannot be considered as clinically relevant as,
besides the technical inadequacy, control investigations with both non-positive
defined healthy and ill individuals have never been published.
The polymerase chain reaction (PCR) is a technique for a manifold multiplication
of short DNA fragments, developed by Nobel prize winner for chemistry,
Kary Mullis. Upon measuring the "viral load" the RNA fragments
in the blood stream first have to be converted into DNA and then multiplied
as such. The single, developing technical steps of this method are prone
to failure. The slightest impurity, drugs, such as heparin and other substances
interfere with a reproducible functioning of the PCR method, especially
with quantification (53). Kary Mullis, the inventor of this method does
not miss any occasion to critizise the application of his technology in
the context of AIDS (52). Further more, it is concealed that it does not
make sense, either practically nor theoretically, to initially multiply
manifold fragments of genetic structure and then to postulate their manifold
presence. In case they were actually present in the blood samples it would
cause no problem to prove their existence by simple, quick and cheap standard
methods (51) and, if de facto, viruses did exist in the blood stream, scientists
certainly would have been successful in making them visible. Hence, up
to date, no scientist claims this achievement, a fact which has been confirmed
under coercive evidence by the German Health Ministry in 1996. After the
report of a produced "positivity" in the "viral load"
during a vaccination test with proteins (54) of a previously "negative"
defined test person it is now frankly admitted that repeated wrong-positive
results in the viral load are quite a wellknown phenomenon (55).
Impairment of energy formation in mitochondria by nucleoside analogues
such as AZT (Azidothymidine, Zidovudine)
AIDS patients quite often demonstrate a weakening of their skeletal
muscles. Up to 1990 this was considered a HI-virus-caused impairment of
muscles. In 1990 DALAKAS et al. demonstrated that this kind of muscle disease
is due to an administration of AZT, weakening the mitochondria within muscle
cells. With the excessive release of free radicals the mitochondria are
affected in their function of forming ATP as key substance in metabolic
energy (56). HAYAKAWA et al., in 1991, demonstrated important changes in
the mitochondrial DNA (mtDNA) in the liver of mice after the administration
of AZT. The final sentence of this paper reads: "However, for AIDS
patients it is urgently necessary to develop a remedy substituting this
toxic substance AZT" (57). These results were confirmed by histochemical
methods in the same year by CHARIOT and GHERARDI (58).
The toxicity of nucleoside analogues in the treatment of viral diseases
was thoroughly dealt with in the following years and, it was proven that
the toxic effect causes multiorganic impairments in heart muscle, brain
and kidney, as well as in liver and pancreas (59). Further, it was shown
that successor drugs of AZT such as ddl and ddC cause the same mitochondrial
Since 1991 it would have been mandatory that not only the pharmaceutical
industry but also the registration authorities seriously consider these
impairments caused by long-term administration of nucleoside analogues
and provide proof of the incoherence of AIDS patients death with this drug
treatment; in general this obligation has been avoided and now they face
upcoming connected liability questions.
HIV-proteases inhibitors: A new therapeutic principle in the prevention
and treatment of AIDS
According to the HIV-model long precursor molecules of proteins along
the multiplication process, have to be cut at certain interfaces in order
to create functional HIV proteins upon which, ultimately, new HI viruses
form. Synthetically produced short protein molecules, reproduced after
the interface to be cut from the precursor protein but which cannot be
cut should, according to the model again, inhibit the natural activity
of the HIV protease and thus prevent the formation of new HI viruses. As
a matter of fact the HIV protease has not been isolated, but has been reconstructed
by genetic engineering upon which it was observed that this enzyme is very
similar to the human digestive enzyme, pepsin of the class of the asparate
The problem of the model is that the one and the very same HIV protease
would have to be cut at completely different interfaces in order to form
functional proteins and, ultimately, HIV. Practically, this is not conceivable
and has been explained as: "enzymes do not have a high sequence specificity"
although it has been postulated that: "a therapeutically applicable
inhibitor has to be specific, and should not inhibit human enzymes of this
class of substance." (61) Considering these explanations of the head
of the chemical department of the scientific laboratories at BAYER's, it
becomes obvious that, theoretically, it is not possible to exactly target
the postulated HIV protease. Further, it is impossible not to interfere
in the cellular processes of integration and disintegration of a variety
of proteins. The inhibition of the active protease in AIDS per se makes
sense. However the pharmacological administration of high doses of distinct
aromatic substances is a non-physiological measure, connected with serious
side-effects which excludes their pharmacological use.
Indeed, up to date, the pharmacological HIV protease inhibitors prove
to be connected with side-effects, which demand the absolute necessity
of their replacements by phyto-therapeutic mixtures. Apart from side-effects
such as kidney stones, damage of the liver, an increase of diabetic impairment
of metabolism, CMV retinitis and haemolytic anaemias these protease inhibitors,
after a short-term administration, also demonstrate a loss of effect on
the inflammatory process which was misinterpreted as a result of an acquired
resistance by HIV as well as an incompatibility with many drugs, especially
with the ones of the group of Cytochrom-P450-inhibitors and inductors (62).
Nutritional possibilities in the prevention and treatment of AIDS
Looking at the formula of structure of the synthetic protease inhibitors,
it becomes obvious that these are artificially produced aromatic compounds.
As we have suggested lately, polyphenols as well as tannins and flavonoids
are phyto-protective substances against harmful external influences. As
aromatic substances, they cannot be synthesized by the animal organism.
The nutritional supply of a variety of phyto-polyphenols to the animal
organism has the function of operating as a redox buffer and rebalancing
oxidative stress conditions with their catabolic alteration of metabolism
to the anabolic-catabolic state of equilibrium (63).
Flavonoids and tannins are effective with respect to:
- 1 Inhibition of lipid peroxidation
- 2 Scavenging of oxygen radicals
- 3 Binding and inactivation of pro-oxidative transition metals such
as Fe and Cu
- 4 Binding of proteins including attenuation of their enzymatic activity
Upon these reductive activities flavonoids and tannins are oxidized
themselves; a well known example is the reduction of vitamin E by vitamin
C or coenzyme Q. These mechanisms are at the beginning of a cascade of
recycling. This example demonstrates, that the multitude of almost 5000
different flavonoids and tannins is used to overcome the oxidative state
of the ex-antioxidative molecules at the end of the cascade of recycling,
by transferring it to a variety of native molecules.
The stress-induced state of catabolic metabolism in AIDS is in the center
of the pathogenesis. The correction of the connected whole body inflammations,
caused by oxygen radicals and protease activation, is a compelling preventive
and therapeutic action which urgently demands the use of phyto-therapeutic
Possibilities and limits of treatment of hepatitis in anti-HIV positive
A symptomlessness and the stress-induced activation of liver inflammation
in healthy individuals are characteristic of parenterally transmitted inoculation
hepatitis (hepatitis B and C). The classic example for this occurrence
is posttransfusional hepatitis caused by blood and blood products of clinically
healthy blood donors. At the occasion of a study, made in the early fifties
at the blood transfusion service of the Swiss Red Cross on recipients of
lyophilized pools of mixed plasma of 50 - 70 healthy blood donors, it was
observed that this caused serious, sometime even lethal hepatitis in many
ill recipients (64-66).
It is emphasized that in a contaminated organism with parenterally transmitted
hepatitis inductors (now called hepatitis B and C), the aim of treatment
has to be reduced to just reach a normal state of health. The administration
of virucide, cytotoxic drugs is not able to eliminate these inductors from
the organism. Proceeding from this knowledge, in Poland, for two decades,
BRZOSKO et al. have been collecting data with the Tibetan prescription
of phyto-therapeutic formula, PADMA 28 (67). They showed that this phenol-rich
plant compound is able not only to reduce the serum level of hepatitis
B antigens in hepatitis B patients but also to augment the serum level
of hepatitis B antibodies. At the same time an amelioration was observed
in these patients regarding their clinical condition and the biochemical
and histological results from their hepatitis. Based on these pioneer results,
today, in patients suffering from chronically active hepatitis, the substitution
with phyto-polyphenolic mixtures has priority over other treatments.
How does the nucleoside analogues treatment of AIDS patients influence
their course of disease?
After having examined 8 reports on HIV positive long-term non-progressors,
who stayed clinically symptomless for over 10 years, we realized, that,
without exception, they had not been treated with nucleoside analogues
(68-75). We consider this as a confirmation of our above-mentioned caution
as to the prophylactic and therapeutic administration of these cell toxics,
originally developed for treating cancer, in the autoimmune course of disease
Nutritional supply of polyphenolic mixtures as basic treatment of
anti-HIV positive individuals and AIDS-patients
As initially showed, a positive anti-HIV test is an indication of an
augmented formation of autoantibodies against cytoskeletal proteins, i.e.
actin. This condition is pathognomonic for chronically active hepatitis.
AIDS, as serious immuno-deficiency-syndrome is the expression of
a persistant hypercatabolic state of metabolism along with a stress-induced
whole body inflammation. A successful treatment of such conditions consists
of the nutritional supply of a sufficient quantitiy of antioxidative and
antiproteolytic phyto-phenolic mixtures, consisting of flavonoids and tannins.
As neither the animal nor the human body are able to synthesize aromatic
compounds they are fully dependent on a sufficient supply of anabolic effective
phyto-polyphenolic mixtures, in order to adjust catabolic states of metabolism.
These mixtures are present in drugs made of teas and spices. Padma 28 proved
to be the most effective one. Additionally, it is recommended to balance
other possible states of deficiency of vital nutritional components such
as polyanions and essential fatty acids.
Completing this review we came across the publication by PADIAN et al.
which remarkably emphasizes the insignificance of heterosexual intercourse
in transmitting "HIV". In this study, extended to 10 years, the
authors say: "male-to-female transmission was approximately eight
times more efficient, than female-to-male transmission and male-to-female
per contact infectivity was estimated to be 0.0009".
Obviously, AIDS is not a viral venereal disease, but an inflammatory
autoimmune process (76).
Address of the authors
Prof. A. HÄSSIG
Prof. LIANG Wen-Xi
Dr. K. STAMPFLI
Study Group Nutrition and Immunity
Dr. H. KREMER
Metzendorfer Weg 36
D-21224 Rosengarten-Tštensen b. Hamburg
Dr. S. LANKA Im Dreieck 8
Germany (a-mail: email@example.com)
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