Response to Jeanne Bergman re: “House of Numbers” Lies about Research
Findings on T Cells Destruction and AIDS*
Eleni Papadopulos-Eleopulos
Valendar F. Turner
John M Papadimitriou
David
Causer
November
2009
There are several issues raised in
Jeanne Bergman’s ““House of Numbers” Lies about Research Findings on T Cells
Destruction and AIDS”. They include the
following:
1.
The relevance to human AIDS of research
done in non-human primates.
2.
The role of T4-cells in immunity.
3.
The role of T4 cells in the causation of
the clinical syndrome, that is, the diseases from which “HIV” positive people
die.
Bergman
states: “The lynchpin of Brent Leung’s
argument in “House of Numbers” that HIV does not cause AIDS is the headline of
a 2007 [September 26] article on ScienceDaily.com that read, “Sudden
Loss Of T Cells Is Not Trigger For AIDS, New Study Suggests.”…Leung, in a
voice-over, intones, “In late 2007, ScienceDaily reported that three
prominent research teams had published papers in the Journal of Immunology,
challenging the theory that the sudden loss of T-cells triggers disease and
AIDS.” Since T cell destruction is understood to be the primary mechanism
by which HIV destroys the immune system, this seems to seriously challenge the
HIV/AIDS paradigm…If the sudden loss of T-cells in HIV positive
individuals can’t explain why people get disease, then there must
be co-factors that cause people to get sick and die. Or, factors that
have absolutely nothing to do with HIV”. According to Bergman House of Numbers “did not accurately represent the
research: notably, it failed to mention
that the research was done with non-human primates” (emphasis in original).
If Bergman thinks findings in
non-human primates cannot be extrapolated to humans then why have “HIV” experts
spent decades doing such research and making their extrapolations? Why have the “HIV” experts been using
non-human primates as a model for human AIDS?
Why do “HIV” experts spend millions of dollars on an AIDS animal model if
the findings cannot be extrapolated to humans?
Is their mission to save the non-human primates? If so, from what? They know better than all of us that the non-human
primates which are the natural host of SIV do not develop SAIDS while infected
either with SIV or “HIV”.
Perhaps we can rely on Jeanne Bergman
advising Donald Sodora, the senior author of one of the three 2007 Journal of Immunology papers, that
findings in non-human primates cannot be extrapolated to humans. She might also ask why researchers continue
to experiment on scarce non-human primates but ignore the non-infectious model involving
repeated, allogeneic immune stimulation reported by Israeli scientists in 1997. “Here we describe
a new condition in mice that closely resembles human AIDS, namely, chronic
lymphoproliferation with dramatic depletion of CD4-positive cells, progressive
impairment of the immune responses, and Kaposi’s sarcoma-like tumors or
terminal B-lymphomas”.1
Bergman claims Leung was wrong
because the non-human primates “rebound from the T
cell destruction caused by the infecting virus, whereas humans generally don’t
when they are infected with HIV. Leung
also ignored the actual Journal of Immunology articles that Science
Daily linked to – which is remarkable since his entire case against HIV’s
causality rests on them”.
Two weeks earlier, on September
11, Science Daily published an article
entitled “SIV Infection of Natural Hosts Provides New Insight Into HIV Disease
Complexity”. In this article Sodora was
quoted as saying: “Our assessment of
these natural hosts like mangabeys offers insight into the disease and shows us
that progression to AIDS likely results from the cumulative effects of HIV/SIV
replication, CD4 T-cell depletion, generalized immune activation and non-CD4
T-cells depletion or dysfunction”.
Obviously Bergman and whoever she is in collaboration with did not read
the Journal of Immunology papers or
the earlier Science Daily article. In
the latter, Jeffery Milush, the senior author of the paper, was quoted
saying: “When we first observed the
dramatic CD4 depletion in all the tissues we examined in these monkeys, we were
concerned that they might begin to exhibit clinical signs of AIDS…But after
more than six years, we are sure that CD4 depletion by itself does not
necessarily result in progression to AIDS”.
Their graphical data show that for the duration of their study, up to
250 weeks, the “dramatic decline” in CD4 cells was permanent. There was no “rebound” – “rebound” is an
invention of Bergman’s. In their paper
Milush, Sodora and their colleagues wrote:
“Therefore,
these data provide a rationale for investigating
multifaceted therapeutic strategies to prevent progression to AIDS, even
following dramatic CD4 depletion, such that HIV+ humans can survive
normal life spans analogous to what occurs naturally in SIV+
mangabeys.2 Hence, despite Bergman’s protestations, the
authors did extrapolate their findings to humans. Which means the original Science Daily September 26 title and commentary was not at all unreasonable.
At Bergman’s request the editorial
staff at Science Daily revised their September
26 article and also changed the title from “Sudden Loss Of T Cells Is Not
Trigger For AIDS, New Study Suggests” to “Progression Of SIV Infection In Monkeys Points To
Differences Between Human And Simian Forms Of AIDS.” According to
Bergman, the revised “summary of the research
clarifies the distinction between the virus in humans and simians”. What is Bergman talking about? “…the virus”
is not the same virus—one is “HIV” and the other is “SIV”. And it is not possible to compare AIDS in
humans and mangabeys for the simple reason the latter do not develop AIDS.
Before
Bergman and her fellow inquisitors rush to also censor the researchers whose
work was discussed in Science Daily
let us remind them that the “evidence-based science” from humans shows that a decrease
in T4 cells “does not necessarily result in progression to AIDS”, that is, the
clinical syndrome. Lymphocyte activation
(T4 and T8) is more predictive for the development of AIDS and death than are
plasma “HIV” RNA levels or CD4+ lymphocytes.3 4 “Although Ethiopians
not infected with HIV-1 do show signs of persistent immune activation and have
lower numbers of naïve cells compared with healthy individuals [and AIDS
patients] from the developed world, they do not develop AIDS-like symptoms”.5 Neither do T4 cells
protect from the clinical syndrome.6-10 In fact increase in
CD4 cells leads to the clinical AIDS syndrome.
“Approximately 10–40% of patients beginning
The
reasons are simple and were known to both Gallo and Montagnier at the beginning
of the AIDS era. Ten years after the
discovery of the existence of T4 and T8 cells it became obvious these cells do not
have unique immunological functions. In
1983 Zagury (one of Gallo’s collaborators) and his colleagues wrote: “Testing functional properties we found that
NK activity was mediated not only by T10+ cells but also, in some cases, by T4+
and T8+ cells. Moreover, TCGF
production, which may reflect helper activity, was mediated not only by T4+
cells. Only the cytotoxic (
In 1988 Göran Möller (an
immunologist from the University of Stockholm) wrote: “There are three good and
several not so good reasons for questioning the existence of suppressor T cells
as a separate T cell subpopulation”.13 Commenting on Möller’s editorial, researchers
from the Pasteur Institute wrote: “It
follows that the difference between these two cell populations concerns their repertoires and, in consequence, their
maturative or activation stages, possibly their differential mechanisms of
activation…As discussed here, even primary populations of lymphocytes may
follow functional rules in vitro that depart substantially from those operating
in vivo, and cells may look and function differently simply because they are
either connected or isolated. In
essence, and this is both more interesting and difficult to approach, it seems
unavoidable that systems (such as the immune) are more than the sum of isolated
clonal activities”14 (emphasis
in original). In 2007 “HIV”/AIDS experts
from the National Centre in HIV Epidemiology and Clinical Research, University
of New South Wales, Australia wrote: “We
believe that CD4 count at AIDS diagnosis could be an insensitive indicator of
association with immune deficiency”.15
In a 1981 commentary in JAMA
entitled: “OKT3, OKT4, and all that”, one reads: “The T- and B-cell measurers – having run
through the sick, the elderly, the young, the pregnant, the bereaved – had
finally run out of diseases. Each
condition was the subject of many reports; so that now, to give but one
example, we can conclude with some assurance that T-cell numbers are up, down,
or unchanged in old folks….And now it’s starting all over again, this time with
T-cell subsets. Think, dear reader, and
grieve, dear editor, about how many investigators are at this very moment
measuring T-cell subsets in systemic lupus erythematosus, in rheumatoid
arthritis, in solid tumours (all different sorts – one article for each), in
lymphomas, in pneumonia, after surgery, after burns, after trauma, in asthma,
in cirrhosis, in Crohn’s disease, in glomerulonephritis, in myositis, in
familial Mediterranean fever, in leprosy, in Dengue fever, after cardiac
transplants, and so on. Meanwhile others
will be out measuring blacks, whites, Orientals, native Americans, men, women,
children, babies, old folk, astronauts, and laboratory technicians. Cells will be garnered and measured from
blood, from lungs, from kidneys, from liver, and from CSF and ascitic
fluid…What can be done to staunch the anticipated outflow?…We might
legitimately ask, why fight? Why not let
us unimaginative immunologists publish to our heart’s content? I will ignore the obvious economic arguments
for fear that they might be taken seriously.
My strongest argument is this:
Measurement of T and B cells and their subsets in diseases has no
clinical meaning…There is a feeling about that T- and B-cell numbers mean
something an immunologic equivalent of an SGOT level or creatinine
clearance…Non-immunologists have naturally assume that any subject occupying so
much journal space must be relevant in some way – a logical but incorrect
assumption”.16 The evidence in the last 25 years, including
that from “HIV”/AIDS, amply confirms Goodwin’s claim that measurement of T
cells and their subsets in AIDS “has no clinical meaning”.17
After a quarter of a century of
the slogan “HIV” infection = T4 destruction (AID) = deadly diseases the
top “HIV” experts (the protagonist “foot soldiers”, to paraphrase John Moore, are
still to wake up to this), realised that the “evidence-based science” shows
that T4 decrease (Acquired Immune Deficiency) does not equal deadly diseases
(S), that is, T4 destruction ≠ S. To
the contrary, the cause of the deadly diseases(s) is immune activation
(stimulation) not immune suppression. In
other words, in the history of medicine there has been no other more harmful
misnomer than Acquired Immune Deficiency Syndrome (S).
Now the “HIV” experts claim that “HIV”
causes immune activation (stimulation) and the equation ”HIV” infection = T4
destruction (AID) = deadly diseases has become “HIV” infection = immune
stimulation (activation) = deadly diseases.
However, despite the development of this new “evidence-based science”
the “HIV”/AIDS experts have been reluctant to change the name AIDS to Acquired
Immune Stimulation Syndrome (AISS). Why?
Nonetheless, they advocate treating these patients with immunosuppressant
agents including steroids and cyclosporin A. 18
The problem for those who still
want to promote the notion that “HIV” has been proven to exist and is the
causative agent of AIDS/AISS, is that at present there is no “evidence-based
science” to prove their claim. To the
contrary.
1.
At the very beginning of the AIDS/AISS
era Montagnier and Gallo accepted that the phenomenon which they claimed
signified the existence of “HIV” cannot be detected unless the cells are stimulated. “HIV” cannot be both the cause and the effect
of immune activation.
2.
Patients belonging to the AIDS risk
groups are exposed to a plethora of stimulating agents regardless of “HIV”. As far back as 1986 Gallo wrote: “the results
revealed a cytopathogenic [cell killing] mechanism that may account for T4 cell
depletion in AIDS patients and suggest how repeated antigenic stimulation by
infectious agents such as malaria in Africa or by allogenic blood or semen, may
be important determinants of the latency period in AIDS”.19 Is it possible that without such antigenic
stimulation the latency period may well be infinite in “HIV” “infected”
individuals?
3.
In 1995 Gallo stated:
“The first thing I can tell you is that we’ve been able to regularly
culture from Kaposi’s tumors what pathologists say is a tumor cell. We asked:
What is the role of HIV in all this? And we found that inflammatory
cytokines...were the very likely initiatory events in creating this cell. We
said, “Oh, the role of HIV is likely to be in increasing these inflammatory
cytokines.” But we have learned – this should be of interest to everybody that
isn’t completely married to HIV – that the inflammatory cytokines are
reportedly increased in gay men even without HIV infection. Inflammatory cytokines are usually promoted
by immune activation, not by immune suppression. So here was a paradox....So the inflammatory
cytokines may be increased by HIV, but I wish I knew what else was increasing
them before a gay man was ever infected with HIV. Maybe it’s nitric oxide, maybe it’s a
sexually transmitted virus, maybe it’s all of them, maybe it has to do with
rimming because it’s immune stimulation with non-specific infections”.20
4.
“This study demonstrated for the first
time that low preseroconversion numbers of CD4 T cells and increased levels of
immune activation were associated with an increased risk to develop AIDS after
seroconversion...In conclusion, our data show that chronic immune activation
and the size of the CD4 T cell pool are critical factors in HIV-1 pathogenesis,
even when measured before seroconversion” 21 (emphasis added).
*www.houseofnumbers.org/HoN_Lies_about_T_Cells.html
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