From: Pat Fallon (pfallon@ptd.net)
Date: Tue Mar 12 2002 - 08:48:48 MST
>>> I am not a doctor either, but I have been a professional bullshit
>>> detector in other fields, and most of this AIDS-is-not-HIV stuff
>>> sets off my alarms pretty heavily.
>> The "bullshit detector" in the field of virology used to be Koch's
>> postulates. Koch's postulates are simply the application of logic
>> to the problem of determining whether a disease is caused by
>> an infectious agent or not.
> Koch's postulates aren't anything like rules of logic; they're just
> a very good method of proving that X causes Y.
I agree that Koch's Postulates are a very good logical method, but I didn't
say they were "rules of logic". I said they were the application of logic to
the problem of determining whether a disease is caused by an infectious
agent or not.
> Absence of such proof does not in any way suggest
> that X doesn't cause Y, just that it hasn't been proven
> to a certain level. But that level is very high--probably
> much higher than necessary to make useful deductions
> and practical cures and treatments.
I would argue otherwise for one main reason. In this case the abandonment of
satisfying Koch's postulates in favor of what replaced it does mark a
dividing line. Actual molecular isolation of a candidate virus was attempted
and it failed [Note A]; it was abandoned in favor of finding surrogate
markers like proteins that are said to be specific to HIV. I would argue
this is not so much a difference in degree, as in proving something to a 95%
level instead of 99%. But instead a categorical difference with more
significance.
It is significant because the evidence cited by Gallo and Montagnier in
place of Koch's Postulates is not nearly rigorous enough to distinguish
between proteins that indicate infection by a common virus, and proteins
that are elicited by the body itself in response to stress or the lab
procedures involved.[Note B]
All of the proteins [and other markers] used as surrogates for molecular
isolation, which are supposedly specific to HIV, are not specific to
HIV.[11]
The proteins detected by the "HIV" test have never been shown conclusively
to be components of a viral antibody, or to be associated specifically with
the cause of anything, as opposed to a possible effect.
This is the heart of the Perth Groups argument with the claims of "HIV
isolation."
Despite all the sophisticated biotechnology and vast investment in virology,
the best evidence for HIV is only by correlation with antibodies present
against it. Or, as stated by the leading English AIDS scientist Robin Weiss
and the CDC's Harold Jaffe, "the evidence that HIV causes AIDS is
epidemiological and virological, not molecular." Gallo emphasizes that point
in his book. He derides Koch's Postulates as outdated. His replacement? He
declares correlation to be "one hell of a good beginning."
And so it can be. But a problem for this method has always been that
correlation does not prove causation.
The time-honored method of avoiding the pitfalls of correlation was to
isolate the candidate virus from the blood of sick patients. Extract
proteins and genetic material from this pure isolate. Re-infect new host
cells, see multiplication of the original viral particles, as confirmed by
re-isolation and redetection of the proteins and genetic material previously
extracted from the candidate.
We abandon Koch's Postulates at our peril. As you are probably aware, they
were adopted due to constant false claims by microbe hunters that they had
found microbes causing diseases. Many of the diseases in question turned out
to be non-infectious, such as scurvy, beriberi, and pellagra, which are all
vitamin deficiency diseases. A more recent example of ignoring Koch's
Postulates was the Japanese "SMON disease", thought throughout the 1960's
and 70's to be caused by a virus, and which was later found to be caused by
a specific medication, clioquinol.
In the mid 1970s Gallo claimed to have discovered the first human retrovirus
in patients with leukemia. He claimed his data proved the existence of a
retrovirus which he called HL23V.[6,7] Now, just as he would later do for
HIV, Gallo used antibody reactions to "prove" which proteins in the cultures
were viral proteins. However, a few years after that these same antibodies
were shown to occur naturally and be directed against many substances that
had nothing to do with retroviruses.[8,9] When the antibodies were shown to
be non-specific, HL23V disappeared. It was realized that HL23V was a big
mistake. There was no HL23V retrovirus. So the Gallo data turned out to be
an embarrassment and HL23V is now extinct. What's interesting for us though
is that the evidence used to claim proof of the existence of HL23V is the
same kind of evidence said to prove the existence of HIV. In fact the
evidence for HL23V was better than HIV. [Note D]
> But that level is very high--probably
> much higher than necessary to make
> useful deductions and practical
> cures and treatments.
If you think a certain marker indicates infection by a deadly virus, you
will make different deductions and develop different treatments than if you
think a certain marker is elicited by the body itself in response to stress
or the lab procedures involved.
If a disease [or syndrome] is not caused by a virus, then anti-viral therapy
will not be helpful, and may in fact be counterproductive or toxic.
Pat Fallon
pfallon@ptd.net
[Notes]
------------------------------------------------------------
[A] Montagnier and his team at the Pasteur Institute tried to get a pure
isolate of his candidate virus. However, despite "Roman effort", they could
see no particles with "morphology typical of retroviruses. I repeat we did
not purify..." [1]
[B] In their papers on isolation, Gallo and Montagnier cite 3 lines of
evidence: detection of reverse transcription activity, detection of
retroviral-like particles in cell cultures, and antibody reactions.
However, reverse transcription activity is not unique to retroviruses, and
in fact RT activity in normal cells is promoted by the very conditions which
Montagnier and Gallo subjected their patients' T-cells to.[2] Therefore,
detection of RT activity in these cultures was not proof that there was a
retrovirus present.
Secondly, Gallo and Montagnier offered as evidence photographs of particles
in impure cell cultures and asserted that not only were they retroviruses,
but they were a specific retrovirus, "HIV." However, as even Gallo
admits,[3] retroviral-like particles that are not infectious are common in
cultures, especially those subjected to the conditions that Gallo and
Montagnier used in order to cultivate "HIV." Pointing to particles in impure
cell cultures that are viral-like was hardly proof that those particles were
a retrovirus, let alone a specific retrovirus, "HIV."
Thirdly, Gallo and Montagnier offered antibody reactions as proof of
isolation of their virus from AIDS patients. They identified certain
proteins in these cultures as "HIV proteins." This was done not by
extracting those proteins from the viral isolate, because there was no viral
isolate. They had a soup containing a few virus-like objects and a lot of
contaminating cellular debris. To decide which proteins extracted from this
mix were from the virus-like objects, they exposed the proteins to blood
samples from both AIDS patients and non-AIDS patients. If a protein caused
an antibody response from an AIDS patient, and no antibody response from a
non-AIDS patient, they said that one was an "HIV protein." These proteins
were then used in the antibody and Western Blot tests. A Positive result is
interpreted as indicating the presence of "HIV antibodies."
However, antibodies cross-react, and AIDS patients have a much higher level
of circulating antibodies than in normal, healthy individuals. Thus AIDS
patients were likely to have antibody cross-reactions with any given protein
more often than non-AIDS patients. Also, false positives may be caused by
vaccinations against other diseases or current or past diseases.[4]
Moreover, antibodies can be raised against a non-viral protein, e.g. that of
endogenous nature (arising from within, not from infection).[Note C]
Identification of certain proteins as "HIV proteins," simply because they
reacted with antibodies of AIDS patients and not non-AIDS patients was
insufficient proof that these proteins were actually from a new virus, "HIV.
[C] Normal human DNA contains retroviral information which did not get there
following a retroviral infection. The cell was born with it.[5] So amongst
all our DNA there are stretches made up of some retroviral information and
that may sit there maybe all your life until something happens. The DNA
starts to make RNA and hence proteins, and this may go even further and lead
to the assembly of endogenous retroviral particles. They're called
endogenous because they're not something that got in from the outside. Like
HIV is supposed to. Something that gets in from the outside is called
exogenous. Long before the AIDS era everyone knew that in animal cells
endogenous retrovirus production could occur spontaneously. You make a cell
culture and do nothing else. Just leave it on the bench for a few days or
maybe a few weeks and then one day it starts to produce retroviral-like
particles. They seemingly come out of nowhere and the process can be
significantly accelerated and the yield of particles increased, sometimes
millions of times, by conditions which induce cellular activation, the same
conditions which are obligatory to obtain what is called HIV from cell
cultures.
Up until 1993, neither Gallo nor Fauci who is another well-known HIV
researcher, accepted that humans contain the DNA to make endogenous
retroviruses but now it's accepted that endogenous retroviral DNA forms
about 1% of human DNA. That's about 3,000 times larger that what the experts
claim is the size of the HIV genome. And what's more, new retroviral genomes
can arise by rearrangements and recombination of existing retroviral
genomes. Furthermore, endogenously produced retroviruses are morphologically
and biochemically indistinguishable from exogenous retroviruses.
[D] In fact, the evidence for the "isolation" of HL23V surpassed that of
HTLV-I and HIV in at least two aspects. Unlike HIV, Gallo's group: (a)
reported the detection of reverse transcriptase activity in fresh,
uncultured leucocytes; (b) published an electron micrograph of virus-like
particles banding at a sucrose density of 1.16 gm/ml, the density which
defines retroviral particles. Following the discovery of HL23V, some
researchers attempted to determine its prevalence utilizing antibody tests
while others were interested to determine the specificity of the antibody
reactions. The latter included one group from the Laboratory of Cellular and
Molecular Biology, National Cancer Institute and another from the Laboratory
of Viral Oncology, Memorial Sloan-Kettering Cancer Center. Using the "viral
glycoproteins", these groups; found that the antibodies present in human
sera which reacted with these proteins were "directed against carbohydrate
structures" and concluded that "The results are consistent with the idea
that the antibodies in question are elicited as a result of exposure to many
natural substances possessing widely cross-reacting antigens and are not a
result of widespread infection of man with replication competent
oncoviruses" (retroviruses). In 1981 Gallo accepted the evidence that the
antibodies, which reacted with the presumed viral proteins of HL23V, were
not so directed "but against the carbohydrate moieties on the molecule that
are introduced by the host cell as a post-transcriptional event, and which
are therefore cell-specific and not virus-specific." [10] This discovery
was of such significance that today nobody, not even Gallo considers HL23V
as being the first human retrovirus, or even a retrovirus.
---------------------------------------------------------------
Footnotes
[1] http://www.virusmyth.com/aids/data/dtinterviewlm.htm
[2] 149. 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. 150.
[3] Gallo, R. C., Wong-Staal, F., Reitz, M., Gallagher, R. E., Miller, N. &
Gillepsie, D. H. 1976. Some evidence for infectious type-C virus in humans.
pp. 385-405, in Animal Virology, edited by D. Balimore, A. S. Huang and C.
F. Fox, Academic Press Inc., New York.
[4] Factors Known to Cause False-Positive HIV Antibody Test Results.
Continuum; 4(3): 5. 64 references to conditions that can cause
false-positive HIV test results.
[5] Lower et al. The viruses in all of us: Characteristics and biological
significance of human endogenous retrovirus sequences. Poc. Natl. Acad. Sci.
USA; 93: pp 5177-5184
[6] Gallo RC, Wong-Staal F, Reitz M, Gallagher RE, Miller N, Gillepsie 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.
[7] 21. Gallagher RE, Gallo RC. (1975). Type C RNA Tumor Virus Isolated from
Cultured Human Acute Myelogenous Leukemia Cells. Science 187:350-353.
[8] 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. U S A
77:1622-1626.
[9] 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. U S
A 77:1617-1621.
[10] Kalyanaraman VS, Sarngadharan MG, Bunn PA, Gallo RC. (1981). Antibodies
in human sera reactive against an internal structural protein of human
T-cell lymphoma virus. Nature 294:271-273.
[11] Papadopulos-Eleopulos E, et al (1997) HIV Antibodies: Further Questions
and a Plea for Clarification. Medical Research and Opinion. V 13: 627-634.
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