HHV-6 and AIDS
The following quotes provide an overview of the role
of HHV-6 in AIDS:
of HHV-6 in AIDS:
"Imagine the consternation created during 1990 by
reports that HIV may be neither necessary nor
sufficient to cause the syndrome. The key experiments
have been performed in the laboratory of the
discoverer of HIV himself, Luc Montagnier of the
Institute Pasteur in Paris. If anyone has a stake in
proclaiming that HIV is the primary cause of AIDS and
that he is the primary discoverer of that cause, it is
certainly Montagnier. Yet Montagnier has announced
that HIV is not sufficient to cause AIDS."
reports that HIV may be neither necessary nor
sufficient to cause the syndrome. The key experiments
have been performed in the laboratory of the
discoverer of HIV himself, Luc Montagnier of the
Institute Pasteur in Paris. If anyone has a stake in
proclaiming that HIV is the primary cause of AIDS and
that he is the primary discoverer of that cause, it is
certainly Montagnier. Yet Montagnier has announced
that HIV is not sufficient to cause AIDS."
The response from most other HIV researchers has been
to ignore Montagnier's data. A few, such as Robert
Gallo, have responded by producing counter claims of
their own. Gallo, for example, has published studies
showing that both HTLV I (one of his earlier
discoveries) and herpes simplex type 6, another virus,
greatly increase HIV infectivity, replication, and
cell killing. He, in other words, thinks that
Montagnier has picked the wrong cofactor.
Wrong or right, the necessity for cofactors to
stimulate HIV activity raises the intriguing question
of whether HIV is actually the cause of AIDS.
to ignore Montagnier's data. A few, such as Robert
Gallo, have responded by producing counter claims of
their own. Gallo, for example, has published studies
showing that both HTLV I (one of his earlier
discoveries) and herpes simplex type 6, another virus,
greatly increase HIV infectivity, replication, and
cell killing. He, in other words, thinks that
Montagnier has picked the wrong cofactor.
Wrong or right, the necessity for cofactors to
stimulate HIV activity raises the intriguing question
of whether HIV is actually the cause of AIDS.
Where we have seen HHV-6A in tissue, we see dead
tissue. And where you see HIV-you know, you can have
HIV alone, and you may see some reactive changes, like
the immune system reacting to a viral infection as if
you have flu or something like that. But you don't see
dead tissue. You don't see destroyed organs and scar
formation, and that's what you see when you see
HHV-6A. We find replacement of the normal architecture
of the lymph nodes with scar tissue. HHV-6A kills it.
It kills the lymph node tissue. If I were to place my
bets--I do think the viruses HIV and HHV-6A are
interactive. I think one of the reasons why you almost
always find both of them is that there are viral
products, some of the gene products that they make,
that enhance each other's replication.
I think they're a team. And, when the two of them are
present, they induce the production of more of each
other. It's a mutually enhancing relationship. It's
our feeling that if you could interrupt or limit or
suppress the HHV-6A infection, the levels of HIV would
go down tremendously and HIV would become just a
chronic viral infection. And, potentially, the
antiviral agents that are out there would be able to
manage that. We don't have any evidence, looking in
the tissue, that HIV is responsible for any of the
destruction. And, if you think about it, HIV infects
patients for years-a decade or more-without
progressing to AIDS. When you look in their tissues,
you have to ask how you can have such a long-term
viral infection and have no damage? Then something
seems to happen somewhere in their course of disease.
In some people, it happens earlier; in some people, it
happens later; and there's that small percentage of
people in whom it never seems to happen at all. Our
hypothesis would be that, if we were to look in the
lymph nodes of the long-term non-progressors, we would
not find HHV-6A.
tissue. And where you see HIV-you know, you can have
HIV alone, and you may see some reactive changes, like
the immune system reacting to a viral infection as if
you have flu or something like that. But you don't see
dead tissue. You don't see destroyed organs and scar
formation, and that's what you see when you see
HHV-6A. We find replacement of the normal architecture
of the lymph nodes with scar tissue. HHV-6A kills it.
It kills the lymph node tissue. If I were to place my
bets--I do think the viruses HIV and HHV-6A are
interactive. I think one of the reasons why you almost
always find both of them is that there are viral
products, some of the gene products that they make,
that enhance each other's replication.
I think they're a team. And, when the two of them are
present, they induce the production of more of each
other. It's a mutually enhancing relationship. It's
our feeling that if you could interrupt or limit or
suppress the HHV-6A infection, the levels of HIV would
go down tremendously and HIV would become just a
chronic viral infection. And, potentially, the
antiviral agents that are out there would be able to
manage that. We don't have any evidence, looking in
the tissue, that HIV is responsible for any of the
destruction. And, if you think about it, HIV infects
patients for years-a decade or more-without
progressing to AIDS. When you look in their tissues,
you have to ask how you can have such a long-term
viral infection and have no damage? Then something
seems to happen somewhere in their course of disease.
In some people, it happens earlier; in some people, it
happens later; and there's that small percentage of
people in whom it never seems to happen at all. Our
hypothesis would be that, if we were to look in the
lymph nodes of the long-term non-progressors, we would
not find HHV-6A.
--Konnie Knox
HHV-6 Researcher
An interview with Neenyah Ostrom in "New York Native"
http://www.chronicillnet.org/online/Knox.html
HHV-6 Researcher
An interview with Neenyah Ostrom in "New York Native"
http://www.chronicillnet.org/online/Knox.html
A microbiologist at the University of California,
Duesberg was relentlessly attacking Gallo's view of
HIV as a killer. The point I had raised in particular
was Duesberg's questioning of Gallo's recent interest
in so-called co-factors that helped HIV overwhelm the
immune system. Anyone who bothered searching for a
co-factor, Duesberg reasoned, was obviously unclear of
the actual cause of a disease.
Duesberg was relentlessly attacking Gallo's view of
HIV as a killer. The point I had raised in particular
was Duesberg's questioning of Gallo's recent interest
in so-called co-factors that helped HIV overwhelm the
immune system. Anyone who bothered searching for a
co-factor, Duesberg reasoned, was obviously unclear of
the actual cause of a disease.
--Nicholas Regush
The Virus Withinpage 20
The Virus Withinpage 20
Although Gallo made a strong effort to encourage
researchers to consider the potential of HHV-6 as a
possible co-factor in AIDS, he could not break down
the resistance to the idea that a common virus could
be such a killer.
researchers to consider the potential of HHV-6 as a
possible co-factor in AIDS, he could not break down
the resistance to the idea that a common virus could
be such a killer.
--Nicholas Regush
The Virus Withinpage 54
The Virus Withinpage 54
Knox was fascinated by how HHV-6, like HIV, attacked
T-4 lymphocytes, monocytes and macrophages.
T-4 lymphocytes, monocytes and macrophages.
--Nicholas Regush
The Virus WithinPage 69
The Virus WithinPage 69
The 34 autopsy samples harvested from nine people who
had died of AIDS were sent from a Milwaukee hopsital
to the Carrigan lab "fixed" in formalin, a
disinfectant and preservative for biological
specimens, and embedded in paraffin. Soon after the
package arrived in the summer of 1993, Konnie Knox
eagerly yet meticulously analyzed each sample by
drawing on elaborate procedures that determine whether
or not a viral infection is active at the time of
death.
In this first phase of her doctoral project since
being admitted to graduate school, Knox was expecting
to find evidence that HHV-6 played a role in the
development of AIDS. It was turning out that he virus
could be awakened in people with immune-system
defects. It stood to reason the same would apply among
AIDS patients. But she did not anticipate just how
much HHV-6 infection she would find.
The results of her experiments gave her a jolt: all 34
tissue samples of lung, lymph node, liver, kidney and
spleen revealed that at the time of death there was
active HHV-6 infection, as opposed to merely a
biological sign that the virus was "latent" (embedded
in the tissue). Since these tissue types had been
provided for almost all the cases, Knox was also able
to determine that the active infection had become
widespread.
had died of AIDS were sent from a Milwaukee hopsital
to the Carrigan lab "fixed" in formalin, a
disinfectant and preservative for biological
specimens, and embedded in paraffin. Soon after the
package arrived in the summer of 1993, Konnie Knox
eagerly yet meticulously analyzed each sample by
drawing on elaborate procedures that determine whether
or not a viral infection is active at the time of
death.
In this first phase of her doctoral project since
being admitted to graduate school, Knox was expecting
to find evidence that HHV-6 played a role in the
development of AIDS. It was turning out that he virus
could be awakened in people with immune-system
defects. It stood to reason the same would apply among
AIDS patients. But she did not anticipate just how
much HHV-6 infection she would find.
The results of her experiments gave her a jolt: all 34
tissue samples of lung, lymph node, liver, kidney and
spleen revealed that at the time of death there was
active HHV-6 infection, as opposed to merely a
biological sign that the virus was "latent" (embedded
in the tissue). Since these tissue types had been
provided for almost all the cases, Knox was also able
to determine that the active infection had become
widespread.
Knox was particularly struck by the magnitude of HHV-6
lung infected tissue. HHV-6 had attacked the lungs of
all nine of the deceased. In one of the six patients
who had died from respiratory failure, the density of
HHV-6 infection was so great that she suspected the
virus was directly to blame. Previously, the cause of
this patient's lung disease had not been diagnosed.
Here was a likely example of how the virus could cause
lethal organ damage in someone with AIDS.
lung infected tissue. HHV-6 had attacked the lungs of
all nine of the deceased. In one of the six patients
who had died from respiratory failure, the density of
HHV-6 infection was so great that she suspected the
virus was directly to blame. Previously, the cause of
this patient's lung disease had not been diagnosed.
Here was a likely example of how the virus could cause
lethal organ damage in someone with AIDS.
--Nicholas Regush
The Virus WithinPage 84
The Virus WithinPage 84
In November 1993, Robert Gallo's lab published data
gleaned from autopsies of five people who had died of
AIDS, demonstrating an abundance of HHV-6 infection.
Footprints of the virus were found in areas such as
cerebral cortex, brain stem, cerebellum spinal cord,
tonsil, lymph nodes, spleen, bone marrow, salivary
glands, esophagus, bronchial tree, lung, skeletal
muscle, myocardium, aorta, liver, kidney, adrenal
glands, pancreas and thyroid.
gleaned from autopsies of five people who had died of
AIDS, demonstrating an abundance of HHV-6 infection.
Footprints of the virus were found in areas such as
cerebral cortex, brain stem, cerebellum spinal cord,
tonsil, lymph nodes, spleen, bone marrow, salivary
glands, esophagus, bronchial tree, lung, skeletal
muscle, myocardium, aorta, liver, kidney, adrenal
glands, pancreas and thyroid.
--Nicholas Regush
The Virus WithinPage 85
The Virus WithinPage 85
The culmination of these efforts came in April 1993,
when scientists at NCI demonstrated in the laboratory
that HHV-6 infects and kills natural killer cells.
these are the immune cells that destroy abnormal cells
in the body, particularly those that are infected by
viruses. HHV-6 is the first virus known to be capable
of targeting and seriously damaging such a vital
element of the immune system's antiviral defenses.
In both the Gallo and Carrigan labs, it did not escape
notice that natural killer cell function is, in
varying degrees, disabled in both AIDS and chronic
fatigue syndrome.
when scientists at NCI demonstrated in the laboratory
that HHV-6 infects and kills natural killer cells.
these are the immune cells that destroy abnormal cells
in the body, particularly those that are infected by
viruses. HHV-6 is the first virus known to be capable
of targeting and seriously damaging such a vital
element of the immune system's antiviral defenses.
In both the Gallo and Carrigan labs, it did not escape
notice that natural killer cell function is, in
varying degrees, disabled in both AIDS and chronic
fatigue syndrome.
Knox sensed that she could break new ground in showing
how HHV-6 behaves in AIDS patients. She knew that the
virus was extremely active at the time of their
deaths. She also had learned it could cause major
damage to lymph nodes during the early development of
AIDS. Now she wanted to know how early such damage
occurred. Could it be even before AIDS was diagnosed?
That would be an eye opener--an unheralded virus
causing damage considered the sole handiwork of HIV.
But such a finding would not come as a shock to Knox,
considering the nodes were loaded with lymphocytes,
the chief targets of HHV-6.
how HHV-6 behaves in AIDS patients. She knew that the
virus was extremely active at the time of their
deaths. She also had learned it could cause major
damage to lymph nodes during the early development of
AIDS. Now she wanted to know how early such damage
occurred. Could it be even before AIDS was diagnosed?
That would be an eye opener--an unheralded virus
causing damage considered the sole handiwork of HIV.
But such a finding would not come as a shock to Knox,
considering the nodes were loaded with lymphocytes,
the chief targets of HHV-6.
Following her instincts, Knox decided to focus on
macrophages, the large scavenger cells that serve as
the lungs' first line of defense against a variety of
infections. Her autopsy-tissue study had already shown
that macrophages were often depleted in the lungs of
HIV-infectd AIDS patiens, and she now wanted to know
how HHV-6 was capable of knocking out those cells. Her
tests showed that, besides destroying macrophages,
HHV-6 interfered with the normal functioning of the
scavenger cells by blocking the release of a type of
oxidant, a substance the cells normally generate to
attack microbes. Knox noted that HIV was not known to
be capable of this specific type of action. She
concluded that, at the very least, HHV-6 could
contribute to the depletion of the macrophages in the
lungs. This in turn woud weaken the immune system,
leaving the body vulnerable to a host of infections
that were normally well controlled.
Did HHV-6 help HIV destroy macrophages in the lungs?
Not necessarily. HHV-6 apparently had the potential to
do a brutally effective job on its own. Perhaps HIV
was giving HHV-6 a boost, not the other way around. Or
more provocative yet, Knox wondered, was HIV doing any
killing in the body, or was HHV-6 the lone assassin?
Clearly, heresy was incubating in the Milwaukee wing
of AIDS science.
macrophages, the large scavenger cells that serve as
the lungs' first line of defense against a variety of
infections. Her autopsy-tissue study had already shown
that macrophages were often depleted in the lungs of
HIV-infectd AIDS patiens, and she now wanted to know
how HHV-6 was capable of knocking out those cells. Her
tests showed that, besides destroying macrophages,
HHV-6 interfered with the normal functioning of the
scavenger cells by blocking the release of a type of
oxidant, a substance the cells normally generate to
attack microbes. Knox noted that HIV was not known to
be capable of this specific type of action. She
concluded that, at the very least, HHV-6 could
contribute to the depletion of the macrophages in the
lungs. This in turn woud weaken the immune system,
leaving the body vulnerable to a host of infections
that were normally well controlled.
Did HHV-6 help HIV destroy macrophages in the lungs?
Not necessarily. HHV-6 apparently had the potential to
do a brutally effective job on its own. Perhaps HIV
was giving HHV-6 a boost, not the other way around. Or
more provocative yet, Knox wondered, was HIV doing any
killing in the body, or was HHV-6 the lone assassin?
Clearly, heresy was incubating in the Milwaukee wing
of AIDS science.
More work in the lab led Knox to further appreciate
the trouble HHV-6 could play in AIDS. She noted that
blood problems are common in AIDS, but the AIDS
scientific community had been far from clear on
whether HIV is actually able to disturb the bone
marrow's normal blood-manufacturing processes. Knox
now wondered whether HIV was really doing anything.
Knox's lab studies demonstrated that HHV-6-infected
marrow cells--not the HIV-infected ones--blocked the
ability of the marrow to produce mature,
differentiated cells.
the trouble HHV-6 could play in AIDS. She noted that
blood problems are common in AIDS, but the AIDS
scientific community had been far from clear on
whether HIV is actually able to disturb the bone
marrow's normal blood-manufacturing processes. Knox
now wondered whether HIV was really doing anything.
Knox's lab studies demonstrated that HHV-6-infected
marrow cells--not the HIV-infected ones--blocked the
ability of the marrow to produce mature,
differentiated cells.
Knox obtained lymph-node biopsies from 10 people
positive for HIV and found that all were actively and
predominantly infected with HHV-6A. She also
discovered the colonization had mostly occurred early
on, as suggested by T-4 lymphocytes counts that were
higher than the cut-off point of 200, which qualifies
someone for an AIDS diagnosis. One HIV-positive
individual's biopsy had even produced a count of 711.
HHV-6 was clearly active and reproducing itself before
AIDS had even been diagnosed.
positive for HIV and found that all were actively and
predominantly infected with HHV-6A. She also
discovered the colonization had mostly occurred early
on, as suggested by T-4 lymphocytes counts that were
higher than the cut-off point of 200, which qualifies
someone for an AIDS diagnosis. One HIV-positive
individual's biopsy had even produced a count of 711.
HHV-6 was clearly active and reproducing itself before
AIDS had even been diagnosed.
--Nicholas Regush
"The Virus Within"
Page 98
"The Virus Within"
Page 98
When Knox studied the brains of six people who died of
AIDS and found extensive damage in four to their nerve
fiber sheaths, she also detected active HHV-6
infection. The infected cells were only in areas where
the damage had occurred and never in healthy tissue.
The damage tissue tested negative for signs of HIV,
CMV, and other microbes. Again, there was only HHV-6.
AIDS and found extensive damage in four to their nerve
fiber sheaths, she also detected active HHV-6
infection. The infected cells were only in areas where
the damage had occurred and never in healthy tissue.
The damage tissue tested negative for signs of HIV,
CMV, and other microbes. Again, there was only HHV-6.
Joseph Sonnabend, the New York doctor who was one of
the first to care for AIDS patients, placed CMV high
on his list of key suspects for his multiple-factor
theory of how AIDS developed. He had studied many gay
men heavily infected by CMV. Donald Francis, a
researcher at the Center's for Disease Control in
Atlanta also advanced CMV as a possible cause of AIDS,
based on evidence that the virus infected the brains
of AIDS patients. . . . Scientists such as Sonnabend,
Francis, and the many others who proposed CMV early n
as a possible cause of AIDS did not have the benefit
of knowing that a similar, but in many ways a more
immune-destructive, herpes virus would soon be
unearthed by none other than Gallo and his NCI team.
What they thought was caused by CMV might at least
sometimes, if not often, have been caused by HHV-6.
the first to care for AIDS patients, placed CMV high
on his list of key suspects for his multiple-factor
theory of how AIDS developed. He had studied many gay
men heavily infected by CMV. Donald Francis, a
researcher at the Center's for Disease Control in
Atlanta also advanced CMV as a possible cause of AIDS,
based on evidence that the virus infected the brains
of AIDS patients. . . . Scientists such as Sonnabend,
Francis, and the many others who proposed CMV early n
as a possible cause of AIDS did not have the benefit
of knowing that a similar, but in many ways a more
immune-destructive, herpes virus would soon be
unearthed by none other than Gallo and his NCI team.
What they thought was caused by CMV might at least
sometimes, if not often, have been caused by HHV-6.
Science is not a democracy, Knox was learning. Science
sometimes punishes people for pursuing the truth.
sometimes punishes people for pursuing the truth.
--Nicholas Regush
The Virus WithinPage 113
The Virus WithinPage 113
The latest results were straightforward yet
provocative: 16 lymph-node biopsies from HIV-positive
patients all contained cells actively infected with
HHV-6A. Twelve of 16 patients who had been diagnosed
with progressive disease had more dense infection than
the four patients who had been diagnosed as having a
stable condition. Knox and Carrigan also found more
dense infection in areas where the lymph nodes were
losing lymphocytes than in areas free of destructive
change or where normal tissue in the nodes was already
being replaced by the formation of scar tissue. HHV-6
was the apparent cause of the destruction of lymphoid
tissue that occurred in these HIV-positive people.
HHV-6 was not only at the scene of the crime, but it
appeared to have committed the crime as well. While
the evidence was not conclusive, it was closer than
Knox and Carrigan had ever come in their detective
work. In contrast, there were no convincing studies
demonstrating that HIV could cause similar pathology.
Studying the findings, Knox and Carrigan looked at one
another and wondered if they'd found a smoking gun.
provocative: 16 lymph-node biopsies from HIV-positive
patients all contained cells actively infected with
HHV-6A. Twelve of 16 patients who had been diagnosed
with progressive disease had more dense infection than
the four patients who had been diagnosed as having a
stable condition. Knox and Carrigan also found more
dense infection in areas where the lymph nodes were
losing lymphocytes than in areas free of destructive
change or where normal tissue in the nodes was already
being replaced by the formation of scar tissue. HHV-6
was the apparent cause of the destruction of lymphoid
tissue that occurred in these HIV-positive people.
HHV-6 was not only at the scene of the crime, but it
appeared to have committed the crime as well. While
the evidence was not conclusive, it was closer than
Knox and Carrigan had ever come in their detective
work. In contrast, there were no convincing studies
demonstrating that HIV could cause similar pathology.
Studying the findings, Knox and Carrigan looked at one
another and wondered if they'd found a smoking gun.
In the meantime, they [Knox and Carrigan] learned that
the scientific paper they had written on detecting
active HHV-6 in the lymph nodes of people with AIDS
would not be published by "The Lancet." Since they
believed that the research presented the smoking gun
that HHV-6--not HIV--was what destroyed lymphoid
tissue in AIDS, the rejection by the journal was a
blow.
the scientific paper they had written on detecting
active HHV-6 in the lymph nodes of people with AIDS
would not be published by "The Lancet." Since they
believed that the research presented the smoking gun
that HHV-6--not HIV--was what destroyed lymphoid
tissue in AIDS, the rejection by the journal was a
blow.
When asked why he has neglected HHV-6 research after
promoting the virus for a couple of years as a likely
co-factor in AIDS, Gallo explained that about the time
that he felt he was making some inroads in HHV-6,
aggressive congressional investigations were looking
into reports that he had mismanaged his scientific
work on HIV. There simply was not enough time to
pursue HHV-6 as much as he would have liked, giving
his ongoing HIV research.
Gallo spoke very generously about what Knox and
Carrigan had accomplished, but he emphasized that they
work in too much obscurity to obtain any funding.
"They have clearly shown that HHV-6 is a powerful
pathogen," Gallo said. "If they were headliners at a
major university it would have made a difference."
In other words, if they had the kind of financial
backing and prestige he had, there would be a lot of
interest in HHV-6.
promoting the virus for a couple of years as a likely
co-factor in AIDS, Gallo explained that about the time
that he felt he was making some inroads in HHV-6,
aggressive congressional investigations were looking
into reports that he had mismanaged his scientific
work on HIV. There simply was not enough time to
pursue HHV-6 as much as he would have liked, giving
his ongoing HIV research.
Gallo spoke very generously about what Knox and
Carrigan had accomplished, but he emphasized that they
work in too much obscurity to obtain any funding.
"They have clearly shown that HHV-6 is a powerful
pathogen," Gallo said. "If they were headliners at a
major university it would have made a difference."
In other words, if they had the kind of financial
backing and prestige he had, there would be a lot of
interest in HHV-6.
She [Knox] won't divulge her views on AIDS science.
for one thing, she and Carrigan do keep an open mind
on HIV. But their research on HHV-6 has taught them
that the virus often appears to be doing what HIV is
supposed to be doing in different parts of the body
such as lymphoid tissue and brain tissue: it is
killing cells. Their research also suggests that HIV
may not always be necessary as a companion to HHV-6
when the herpes virus is destroying tissue. But even
suggesting this in writing would raise the hackles of
HIV researchers. In fact, some AIDS scientists compare
any questions of the HIV hypothesis, as it currently
stands, to denial of the Holocaust. With such emotions
running strong in AIDS science, why take a chance of
boldly presenting alternative hypotheses?
for one thing, she and Carrigan do keep an open mind
on HIV. But their research on HHV-6 has taught them
that the virus often appears to be doing what HIV is
supposed to be doing in different parts of the body
such as lymphoid tissue and brain tissue: it is
killing cells. Their research also suggests that HIV
may not always be necessary as a companion to HHV-6
when the herpes virus is destroying tissue. But even
suggesting this in writing would raise the hackles of
HIV researchers. In fact, some AIDS scientists compare
any questions of the HIV hypothesis, as it currently
stands, to denial of the Holocaust. With such emotions
running strong in AIDS science, why take a chance of
boldly presenting alternative hypotheses?
--Nicholas Regush
The Virus WithinPage 224
The Virus WithinPage 224
Knox and Carrigan, while aware of the issues, want no
active part of this often hostile debate. They can't
see that it holds any immediate consequences, one way
or the other, for their scientific work on HHV-6. They
will continue to document their findings and make an
all-out effort to get the data out. Then their
scientific peers can judge for themselves. If in the
end, they won't make a dent in the current HIV theory,
then it won't be for a lack of solid HHV-6 data. And
furthermore, HHV-6 is much more than a virus that
appears to play a powerful role in AIDS. They have
tracked it step by step through a host of other
trouble that it causes in the bone marrow, lungs and
brain tissue of transplant patients. It's active in
the blood of up to 70 percent of people with chronic
fatigue syndrome that are tested. And Knox and
Carrigan also find it active in the blood and brain
tissue of people with MS.
active part of this often hostile debate. They can't
see that it holds any immediate consequences, one way
or the other, for their scientific work on HHV-6. They
will continue to document their findings and make an
all-out effort to get the data out. Then their
scientific peers can judge for themselves. If in the
end, they won't make a dent in the current HIV theory,
then it won't be for a lack of solid HHV-6 data. And
furthermore, HHV-6 is much more than a virus that
appears to play a powerful role in AIDS. They have
tracked it step by step through a host of other
trouble that it causes in the bone marrow, lungs and
brain tissue of transplant patients. It's active in
the blood of up to 70 percent of people with chronic
fatigue syndrome that are tested. And Knox and
Carrigan also find it active in the blood and brain
tissue of people with MS.
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.
