An excerpt from THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP

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Thursday, September 29, 2005

Gallo on HHV-6

Here's what Robert Gallo had to say about HHV-6 in an
NIH interview in 1995:
Have we ever argued for a possible cofactor? Yes, with
the qualification I just told you, that it is obvious
that some things will promote progression and some
things will inhibit progression. One of those things
may be the genetics of me versus you. We can say dose
is a factor that can lead to progression, or lack of
it, and at a greater or lesser rate. But we have
argued for certain herpesviruses as possibly being a
factor in promoting AIDS progression. Several groups
have argued for cytomegalovirus because it does do
things and it does activate more HIV in some subtle
settings.
In the middle of the 1980s, we became aware that the
lymphomas that were associated with HIV infection were
perhaps one-third of the time EBV-positive.
Epstein-Barr virus, as you know, can immortalize some
B cells and, when you have EBV-positive lymphomas,
generally they are the kind of lymphomas that, more or
less... If they do not require EBV, EBV makes the
probability of getting a lymphoma much greater,
because the cell cannot die easily. It is
immortalized. Other genetic events are needed to
develop the lymphoma, but the immortalization of the
cell is perhaps a key factor that makes it probable
that it will be an EBV-containing cell that is the one
that will become a lymphoma.
What about the two-thirds of lymphomas in HIV-infected
persons that were not EBV-positive? We wondered if
there were herpesviruses yet to be discovered. We
looked in the B-cell lymphomas of patients with AIDS
who were negative for EBV and we discovered the first
new herpesvirus in 25 years, and the first herpesvirus
of man that targeted predominantly the T cell.
We had a new herpesvirus, but it was not involved in
the lymphoma, at least not as far as anybody knows,
even today. We even misnamed it. We called it HBLV,
because we found it in a B-cell lymphoma. Then we
studied it more intensively and determined that it
primarily infected T cells, not B cells, which was an
unexpected finding. We learned that it killed T cells
when it replicated. Then we learned that it infected
natural killer cells and, when it did so, it made
those cells attack other natural killer cells. We
learned that it could infect the same cell as HIV and
activate HIV expression. Next we learned that it
infected CD8 cells and activated the gene for CD4, the
only known biological agent I am aware of that
activates the gene for CD4. Now, the CD4+/CD8+ cells
could be targets for HIV.
It was at that stage we proposed that the herpesvirus
might be a cofactor for progression of AIDS. It was
then that I started to be careful of the use of these
words and called it a catalyst for progression, that
is, a nonessential cofactor, but something that makes
disease progression go faster and also makes it more
probable that immune deficiency will develop.
We put that idea out and it got a little bit of a
reception by [Dr. Larry] Corey in Seattle, and by [Dr.
Donald] Don Carrigan at Wisconsin. But then [Dr.
Harold] Jaffe published a paper, the data of which we
already had in hand. I think that paper by Jaffe and
his colleagues at the CDC [Centers for Disease Control
and Prevention] was not a sophisticated look at the
problem. Namely, they said, Look, everybody has
antibody, so how can it be a factor in progression?
That is like saying a cytokine like TNF [tumor
necrosis factor] is not important in disease
pathogenesis because everybody has it. The question
is, if 90 percent of the human population has it, they
also have EBV, but EBV can cause Burkitt's lymphoma
under certain settings. The question is, does it get
activated in an immune-suppressed individual?
We put the problem aside for a while because we did
not have a quantitative assay to measure the amount of
herpesvirus; only this antibody that indicated a
previous exposure to the virus, which everybody
showed. We argued, however, when we presented it, that
we needed to have a quantitative assay for virus in
blood and the amount of human herpesvirus-6 [HHV-6]
DNA in lymphocytes circulating around.
At this time we learned of Carrigan's work. He
reported in a few clinical papers, that sometimes in
immune-suppressed people, following transplantations,
he saw an enormous amount of human herpesvirus-6
replication and that he believed it was responsible
for some of the bone marrow abnormalities in such
people. He showed a lot of virus in bone marrow.
Second, he pointed out and emphasized that
interstitial pneumonia is the cause of death in 10
percent of the deaths of HIV-positive people. No one
knows the cause of that interstitial pneumonia, and he
found the lungs of those who died loaded with human
HHV-6. He presented at our laboratory meeting that he
thought it was very likely that HHV-6 was the cause of
those deaths.
Meanwhile, before this, Japanese workers had shown
that HHV-6 was the cause of roseola infantum, also
known as exanthem subitum, a disease of infants, with
fever and rash, but usually with not much more.
So now what is new? I have discussed with my colleague
[Dr.] Paolo Russo that the only way we are going to
get any proof of this, or get stronger support, is if
we get a specific inhibitor that does not inhibit HIV,
inhibits HHV-6, and as far as we know does not inhibit
anything else, is relatively non-toxic, and then show
that patients do better rather than worse.
Another way of doing it would be to find an animal
model not infected with a parallel virus to HHV-6
which can be infected by SIV [simian immunodeficiency
virus]. SIV can induce some immune deficiency–not the
acute sort–but there are monkeys in which SIV induces
nothing, there are monkeys in which some strains of
SIV induce an acute AIDS, and there are monkeys where
some strains of SIV induce a disease more similar to
the human disease, where it takes time.
We used such a system. This is not published data.
With the SIV alone, there was a little immune
deficiency, and with the HHV-6 alone nothing, but with
the two together they got it. I think we have proven
the point with that rhesus virus and that we can
publish that soon. So, I believe human herpesvirus-6
is a factor in AIDS progression.
http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html


If HHV-6 is the real cause of AIDS, here are some of the implications:

1. HIV is a massive scientific fraud. Something akin to a Ponzi scheme. Scientists who challenged the HIV theory of AIDS (the ones who have been thuggishly censored and silenced) turn out to be on the money.

2. Chronic Fatigue Syndrome and Autism (and many other so-called HHV-6 related mysterious epidemics) are part of the so-called AIDS epidemic.  Chronic Fatigue Syndrome and Autism both are clearly the results of the ravages of HHV-6.

3. AIDS and Chronic Fatigue Syndrome has been artificially and politically separated into two epidemics. We are living in a period of CFS/AIDS apartheid. So-called AIDS patients have to sit in the back of the HHV-6 epidemic bus while the befuddled HHV-6/CFS patients and HHV-6/Autism victims sit up front. Nobody is well-served.

4. AIDS is not a sexually transmitted disease. That paradigm has set a scapegoating and antigay agenda in place that the public thinks is solidly based on science. It is only based on homophobic and racist nosology, epidemiology and virology. The scientists behind the paradigm are charlatans and crooks.

5. The Centers for Disease Control in Atlanta and the Pasteur Institute in Paris have a great deal in common with the institutions of Nazi medicine. For Blacks, everything these institutions have done in the name of AIDS really constitutes a second Tuskegee Syphilis Experiment.

Elements of a Scientific Ponzi Scheme like the Montagnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up

A scientific Ponzi scheme begins with a central seminal or foundational scientific fraud and is  sometimes built on an infrastructure of smaller scientific frauds. Like the fake dividends issued in a strictly financial Ponzi scheme, a scientific Ponzi scheme issues fake dividends in the form of ongoing fraud-based research often framed as "breakthroughs" and bogus extrapolations which make it look like everything is above board and that what, in reality, is scientific fraud, appears to the rest of the scientific community and the public as good faith progress.

A classic scientific Ponzi scheme like the Montgnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up include elements like these:

1. Nosological fraud.

2. Epidemiological fraud.

3. Virological fraud.

4. Treatment fraud.

5. Public health policy fraud.

6. Concealment of negative scientific data and paradigm-challenging anomalies.

7.  Use of an elite network of "old boys" and pseudo-activist provocateurs to censor critics and whistleblowers.

8. Chronic obscurantism.

9. If necessary, vigilantism and witch-hunts against any intellectuals, scientists, or citizens who constitute any form of resistance to the Ponzi scheme.

10. A subservient scientific press that is used as a conveyor belt for the Ponzi scheme's propaganda.

Everything always looks like it is working perfectly in a Ponzi scheme, until the moment comes when someone look at the books and blows the whistle.  Hopefully, that game-changing moment for the Montagnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up is coming soon.


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