The Story behind The Lady Upstairs

Sunday, June 30, 2013

The T-cell Killer HHV-6 May Not Even Need HIV to Destroy The Cells That Prevent Opportunistic Infections

by Neenyah Ostrom
NEW YORK NATIVE/May 22, 1995

What sets off the cascade of events that results in the destruction of the immune systems of "AIDS" patients? Although the putative causal agent of the syndrome, HIV, is believed to orchestrate the immune system's collapse, no one has been able to explain how it does it. Meanwhile, another virus, Human Herpes Virus 6 (HHV-6), has been found to kill immune system cells directly-including T-cells, the loss of which is the agreed-upon hallmark of the syndrome-without any mystery or putative indirect mechanisms that have been attributed to HIV. Now, new research from Robert Gallo's National Cancer Institute of Tumor Cell Biology reveals that HHV-6 infection is required for HIV to be able to infect some T-cells.
Not only is HHV-6 able to infect and kill these T-cells that HIV is unable to infect, these are the very T-cells that are meant to defend against HHV-6 infection. Therefore, HHV-6 is able to elude detection by the immune system by killing these cells. Furthermore, these particular T-cells killed by HHV-6 are also the ones that protect against specific types of bacteria, including the Mycobacterium that causes tuberculosis.
In other words: According to this new research, HHV-6 is not only able to elude detection by the immune system by killing the cells that are meant to defend against the virus, but HHV-6 infection may also be the driving force behind the tuberculosis epidemic that is sweeping the inner cities of the nation.
This research from the National Cancer Institute italicizes the public health tragedy that has been allowed to develop, as billions have been spent unsuccessfully to fight HIV, and very little attention has been paid to HHV-6. HHV-6 is a treatable infection, when it is caught early; it can be controlled by the readily-available drugs foscarnet and ganciclovir, as well as the experimental (and presumably less toxic) drug Ampligen.
But because of the power of the HIV lobby in doling out grant monies, nearly all the anti-"AIDS" research in the U.S. has focused (unsuccessfully) on HIV and on developing (ineffective) anti-HIV drugs.
A collaboration between Paolo Lusso from Gallo's NCI lab and others at the National Institutes of Health examined the "potential role of HHV-6 in AIDS," which is described in their new research report.(1)
These investigators found that the HHV-6 infects a particular subset of T-cells that is "involved in the protective immune response against specific microorganisms"-including HHV-6 itself.
HHV-6 (Variant A) is not only able to infect this subset of T- cells, infection by HHV-6 results, in laboratory studies, in "massive cell death."
In addition to infecting and killing these T-cells, HHV-6 radically alters them: It causes them to secrete the cell surface protein that turns them into CD4 (T4) cells.
This, according to Lusso and colleagues, renders these T-cells newly "susceptible to productive infection by HIV-1."
In other words: HIV is incapable of infecting these T-cells unless HHV-6 has infected them first. (Because of the damage HHV-6 is capable of causing without HIV, one is tempted to say: So what?)
This subset of T-cells has only recently been described, and is called "gamma/delta T-cells."
"These results demonstrate that gamma/delta T-cells can be directly targeted and killed by a herpesvirus and may have implications for the potential role of HHV-6 in AIDS," Lusso and colleagues reported.
This finding raises the question: What is the primary immunosuppressive infection in "AIDS" patients? Is HHV-6 simply loosening the jar's lid so that HIV can remove it?
Or is HHV-6 actually the primary infection that destroys the immune systems of "AIDS" patients?
And if it is, what is this virus doing in other people with active HHV-6 infections-like Chronic Fatigue Syndrome patients?
Lusso is joined in this investigation by NCI colleagues Alfredo Garzino-Demo and Richard W. Crowley, as well as Mauro S. Malnati from the National Institute of Allergy and Infectious Diseases. Their study is published in the April issue of the Journal of Experimental Medicine.(2)
Lusso and colleagues' investigation delves into an arcane and newly-discovered pocket of immunology. It has recently been discovered, they note, that there are two distinct lineages, or families, of T- cells. One is called alpha/beta; the other is called gamma/delta. These two families of T-cells respond to challenges by infectious agents in different ways, which have not yet been entirely elucidated.(3)
The gamma/delta T-cells appear to be capable of responding to viruses, bacteria, and protozoa. In addition, in the laboratory, these T-cells are activated by proteins created in response to an infection- i.e., by the host response, not simply the invading organism itself.
Lusso and colleagues hypothesize that, in living organisms (as opposed to in the laboratoy), these cells' response "to microorganisms may be, at least in part, secondary to the effects that the infection induces in the host, suggesting a possible role of gamma/delta T-cells in the regulation of the immune response and/or in self-reactive immune phenomena."(4)
In other words: Because these cells react to an organism's response to infection, they may play a role in regulating such immune responses to invaders such as bacteria and viruses.
Additionally, it is primarily the gamma/delta T-cells; so, by killing those cells, HHV-6 can elude attack by the immune system.
Lusso and co-authors point out that HHV-6 was the first "T- lymphotropic human herpesvirus" to be discovered. Unlike its close relative HHV-7, HHV-6 is quite deadly to the cells it infects, not only T-cells but also natural killer (NK) cells, B-cells, and monocytes.
Lusso and co-authos put this all into perspective this way: " In all these cell types, HHV-6 induces dramatic cytopathic changes, suggesting that it may act as an immunosuppressive agent in vivo. Moreover, a series of positive viral interactions has been documented between HHV-6 and HIV, the causative agent of AIDS, leading to the hypothesis that HHV-6 may accelerate the natural course of HIV infection in coinfected patients. This concept has been corroborated by the recent demonstration that HHV-6 infection is active and widespread in terminal AIDS patients. Diverse anomalies of both the cellular and humoral arms of the immune system have been reported in patients with AIDS, including gamma/delta T-cell alterations. In this study, we have investigated the susceptibility of gamma/delta T-cells to infection by HHV-6 and the interactions between HHV-6 and HIV in gamma/delta T-cells.(5)"
In their laboratory studies, Lusso and colleagues separated out a population of gamma/delta T-cells (contamination by alpha/beta T-cells was estimated to be less than one percent) and exposed them to HHV-6. After three days, there were signs that the T-cells were infected. After four to seven days, "a growing proportion of gamma/delta T-cells exibited the typical HHV-6 induced cytomorphological changes, consisting of size enlargement, refractile appearance, and loss of blastic shape with the acquision of an evenly rounded cellular profile," according to Lusso et al. "Eventually, the viral cytopathic effect induced widespread cell destruction, resulting in the extinction of the cultures at day 10-12 after infection."(6)
In about 12 days, then, HHV-6 infection resulted in the total destruction of the cell cultures into which the virus was introduced.
Before killing the infected gamma/delta T-cells, HHV-6 decreased the ability of those cells to kill invaders. This loss of function in the T-cells occurred in two to four days.
In other words: Not only does HHV-6 kill these T-cells, it destroys the immune system mechanism that is supposed to kill other invaders.
Gamma/delta T-cells do not ordinarily have the CD4 protein on their surfaces. HHV-6 infection, however, causes them to express this cell surface protein. After nine days of infection, more than 70 percent of the gamma/delta T-cells were expressing the CD4 protein, according to Lusso and colleagues.
HIV uses the CD4 cell protein to infect T-cells. Gamma/delta T- cells are generally resistant to HIV infection. When Lusso and colleagues exposed the HHV-6 infected gamma/delta T-cells (which were producing the CD4 protein) to HIV, however, "they became susceptible to productive infection by HIV-1," they found. When the cells were treated with a substance that inhibited the production of the CD4 protein, HIV was no longer able to infect the cells, "conclusively demonstrating that the HHV-6 induced CD4 was essential for infection of gamma/delta T-cells by HIV-1."(7)
In other words, HIV couldn't even infect these T-cells unless HHV- 6 already had infected them and begun the process of causing their "extinction."
The infection of gamma/delta T-cells by HHV-6 is particularly diabolical, since those cells help to defend against invasion by the virus. By infecting these cells, Lusso and colleaues write, "HHV-6 may seek to escape the immune control of the host and thereby establish persistent infection." They note that HHV-6 "can infect and kill several critical elements of the immune system," suggesting the virus "may have broad immunosuppressive effects."(8)
And, in what may be an even more sinister development, Lusso and colleagues suggest that it is HHV-6, not HIV, that is driving the tuberculosis epidemic.
While HHV-6 has been shown to be associated with potentially life- threatening conditions such as encephalitis, pneumonitis, and bone marrow suppression, in "AIDS" patients, "HHV-6 has been suggested to play a more substantial pathogenetic role," according to Lusso and co- workers.
For instance, "Diverse clinical and experimental observations indicate that HHV-6 may contribute, directly or indirectly, to the destruction of CD4-positive T-cells, a pathological hallmark of AIDS, and thereby expedite the course of the disease."(9)
In particular, "Damage to gamma/delta T lymphocytes could predispose patients to infection by specific microorganisms that these cells help to control, including some (e.g. Mycobacteria [that causes tuberculosis]) that are in important cause of morbidity and mortality in AIDS."
Lusso, along with Gallo, has previously suggested in the medical literature that HHV-6 may play a more primary role in causing "AIDS" than is generally appreciated.
In the March 5, 1994, issue of The Lancet, Lusso and Gallo wrote an editorial that accompanied a research report by Medical College of Wisconsin researchers Konstance K. Knox and Daniel R. Carrigan. Knox and Carrigan noted that "HHV-6 has been proposed as a cofactor in the pathogenesis of AIDS." They decided to evaluate "the frequency of active HHV-6 infections in patients who died with AIDS."(10)
Knox and Carrigan found that 100 percent (34 of 34) of the autopsy tissues from "AIDS" patients tested were positive for HHV-6 infection, compared to only nine of 34 positive for cytomegalovirus infection.(11)
Knox and Carrigan found HHV-6 infections in the lungs, kidneys, livers, spleens, and lymph nodes of the patients studied. They suggested that HHV-6's ability to infect lymphocytes could not only help spread infection throughout the body, but also contribute to the destruction of lymphocytes in "AIDS" patients: "An HHV-6 infected lymphocyte within an area of inflammation could transfer infection to other lymphocytes newly recruited into the lesion which, when combined with immunosuppressive result of CD4 lymphocyte destruction by the HHV- 6 infection, could perpetuate inflammation and lead to significant systemic consumption of lymphocytes."(12)
In their accompanying editorial, Lusso and Gallo point out "That HHV-6 could contribute to the striking depletion of CD4 T-cells seen in patients with AIDS was suggested by us more than five years ago. We made this proposal after observing that HHV-6, unlike cytomegalovirus or other putative cofactors in AIDS, shares with HIV a primary tropism for CD4 T-cells and can productively coinfect with HIV individual target lymphocytes, causing accelerated cytopathic changes..."(13)
Because of all the destruction HHV-6 is known to be able to inflict on the immune system, Lusso and Gallo suggest that "it may have detrimental effects on the immune sytem and expedite progression of the disease [AIDS]."(14)
Is HHV-6 merely "expediting" the progression of "HIV disease," as these HIV investigators suggest?
Or, as HHV-6 researchers like Knox and Carrigan have been showing, is HHV-6 infection more primary to "AIDS" than has been previously acknowledged?
REFERENCES
  1. Lusso, Paolo, Afredo Garzino-Demo, Richard W. Crowley, and Mauro S. Malnati; "Infection of Gamma/Delta T Lymphocytes by Human Herpesvirus 6: Transcriptional Induction of CD4 and Susceptibility to HIV Infection"; Journal of Experimental Medicine 181:1303, April 1995.
  2. Ibid.
  3. Lusso et al., op cit.
  4. Lusso et al., op cit.
  5. Lusso et al., op cit.6. Lusso et al., op cit.
  6. Lusso et al., op cit.
  7. Lusso et al., op cit.
  8. Lusso et al., op cit.
  9. Knox, Konstance Kehl and Donald R. Carrigan; "Disseminated Active HHV-6 Infections in Patients With AIDS"; The Lancet 343:577, March 5, 1994.
  10. Ibid.
  11. Knox and Carrigan, op cit.
  12. Lusso, Paolo and Robert C. Gallo; "Human Herpesvirus 6 in AIDS"; The Lancet 343:555, March 5, 1994.
  13. Ibid.
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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.



Dr. Konstance Knox explains why HHV-6 may be the key to dealing with AIDS.

by Neenyah Ostrom
New York Native, issue #678, April 15, 1996

Konstance Knox, Ph.D., is an HHV-6 researcher who has just published a study with extraordinary implications for AIDS research and treatment strategies. Along with colleague Donald R. Carrigan, Ph.D., Knox demonstrated that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6 Variant A infections in their lymph nodes early in the course of their disease. Seventy-five percent of these patients, in fact, had CD4 cell counts higher than 200 (the cut-off for receiving a diagnosis of AIDS), up to as high a CD4 count as 700. This finding led Knox and Carrigan to conclude that "active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that the A variant of HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS." This new study, in other words, presents data further implicating HHV-6, particularly Variant A (HHV-6A), as a cofactor (at the very least) in the development of AIDS. (The report is "Active HHV-6 Infection in the Lymph Nodes of HIV Infected Patients: In Vitro Evidence That HHV-6 Can Break HIV Latency," published in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology," April 1, 1996.) Knox, who has a Ph.D. in Experimental Pathology from the Medical College of Wisconsin, is currently conducting cancer research in the Immunotherapy Program at St. Luke's Medical Center in Milwaukee, Wisconsin. She spoke to the Native on the day following publication of the new study.
Neenyah Ostrom: What is the bottom line, with respect to your new findings? Is it that Human Herpes Virus 6 (HHV-6) is present from the beginning of what we define as AIDS?
Dr. Konstance Knox: HHV-6 is present from very early in HIV infection. So we're not talking about waiting until people have opportunistic infections, and CD4 counts between 100 and 200. We're finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB. The only opportunistic infections that you see in AIDS patients with CD4 counts above even 100 are TB and Herpes simplex and Herpes zoster. And all three of those, of course, also infect healthy people and cause disease. So, what we found, when we examined the lymph node biopsies of HIV-infected patients, was HHV-6. We found both variants of HHV-6-HHV-6A and HHV-6B-but the predominant virus was HHV-6A. And we're talking about finding the virus in lymph nodes of patients with CD4 counts of over 700. The mean CD4 count of 75 percent of the patients we examined was approximately 300. (There was a total of ten patients in this study just published, and we had CD4 counts on eight of them.) That's a unique finding. And one of the patients had a CD4 count of 711. So why is that virus, HHV-6A, there? My personal impression, because of where we find HHV-6A-we find a predominance of infection in the germinal center of the lymph node, which is where we know HIV hangs out-is that the tat protein of HIV stimulates HHV-6A replication. And in the study that we have just published, the one that came out yesterday [April 1], we showed that HHV-6A causes an increase in HIV production. These findings are not based solely on this one study. We have done subsequent studies, and there is another already-published study by Charles Wood from Miami also demonstrating that tat protein from HIV induced more HHV-6A production. So the theory-what seems reasonable to us-is, because these viruses hang out in the same place, and they infect the same cells, that it's not an accident that they co-localize-where you find HIV, you find HHV-6A. I think that there is a mutual enhancement and potentially almost a mutual dependency for efficient replication. My impression is that HIV kind of acts as a wet nurse to HHV-6A, because in all the other immunocompromised patients that we have looked at-and primarily, these are bone marrow transplant patients-we don't find the A variant of the virus. We don't find it, and the best guestimates of how many people are infected with type A-well, the numbers are sketchy. Because of the blood tests previously available, we only know about type B. You know, the classic numbers are that 90 percent of people by the age of two are infected with HHV-6. But that's the B variant, not the A variant. And the best estimate, up to about the age of 12, is that about five to 15 percent of people are infected with variant A. The epidemiology of HHV-6A infection has not been done. Now, it's kind of curious to me why the studies have not been done. You know, there's been a lot of sort of pooh-poohing about the role of HHV-6 in AIDS. I think that's because people look at it, and they say, well, everybody's infected with HHV-6 by the age of two. Yes, everybody's infected with the B variant. But we don't know how many people are infected with the A variant. We've just completed a study that we have submitted in which we examined 22 HIV-positive and AIDS patients. Every one of them has active replication of HHV-6A and it doesn't matter what stage of disease they're in, from frank AIDS, to autopsies, all the way up to people with CD4 cell counts of over 700. We believe there is a special interaction between HIV and HHV-6A.
N. Ostrom: How different are variants B and A from each other?
K. Knox: Do you mean biologically?
N. Ostrom: Yes. I've heard speculation that they should have been classified as two different viruses, or that, conversely, HHV-7 is no more different from the two HHV-6 variants than they are from each other.
K. Knox: HHV-7 is probably more akin to HHV-6B. There was an interesting study-and it was a PCR [polymerase chain reaction, i.e. "DNA amplification"] study-which basically showed that, if you were to analyze peripheral lymphocytes, you can find HHV-7 and HHV-6B in about 83 percent and 25 percent of healthy people, respectively. HHV-6A is found much, much less frequently. We're talking about a very small percent-five percent of people. HHV-6A is different. Probably a general rule of thumb is that HHV-6A can do everything that B can do, and more. And it's also much more destructive. It is a very destructive virus. It's more similar to what people think of when they think of a herpes virus. It is very lytic-it kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow. In all the dozens to hundreds of transplant patients we've looked at, if we find HHV-6 disease, it's variant B. We have only seen HHV-6A in, I think, five different individuals, from whom we've isolated it or stained it in tissues. These are not HIV-positive individuals. So, we found HHV-6A in five out of 100 or so patients. Four of those patients were dead. It is very destructive.
N. Ostrom: The question then becomes, in my mind, can HHV-6A do everything that HIV can do?
K. Knox: As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV. And these are data from many people's laboratory studies, and that includes Paolo Lusso and Robert Gallo, as well as our own. 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.
N. Ostrom: Do you have plans to do that study?
K. Knox: Well, last December I contacted Giuseppe Pantaleo-he's with Tony Fauci's group [at the National Institutes of Health], who had published the New England Journal of Medicine paper just about a year ago on the progressors and long-term non-progressors and the difference in the lymphoid organs between the two. The basic difference is, in the non-progressors, even though they have replication-competent HIV, they don't have any evidence of degeneration or destruction of their tissue, even though HIV is there. So the hypothesis would be that those few percentage of HIV-infected patients that are long-term non-progressors don't have HHV-6A replicating in their lymph node tissues. Pantaleo has agreed to send us what the NIH has in the way of tissues from that study. Now, I've been waiting-you know, they had the furlough, and all this other kind of stuff. And then I met with Dr. Pantaleo, actually, about the middle of February, and he again reiterated that he would be sending those tissues to me. Thus, he has personally assured me, but, until I have the tissues, we can't do the direct test of the hypothesis.
N. Ostrom: Why can't we get more funding for this research?
K. Knox: Well, I don't know if you've been tracking the kinds of exposes that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there's been a real resistance to entertaining hypotheses or directions of AIDS research that aren't looking specifically at HIV, and that is the basic problem. Our studies themselves have been enthusiastically received, but the funding hasn't followed. And that is funding through the federal agencies-like the NIH-and I think one of the things that has stopped that has been the confusion with HHV-6B. People think, well, if everybody's infected with HHV-6, why doesn't everybody have AIDS? Well, we're all infected with HHV-6B, but there's probably only a very small percentage of people infected with HHV-6A. And there's a very unique relationship between A and HIV-when we examine HHV-6B and HIV together, we don't see the same effects. They don't have the same interaction. So, we're talking about two different viruses, essentially, A and B. And people have merged the two into just HHV-6 and have not appreciated the biologic differences between the two viruses. And actually, in our own research, this has only been clarified in the last year. In our earlier studies, we only had reagents to look at HHV-6. We did not have the specific reagents to separate the two when we looked in the tissue; we could not tell if it was A or B. It's only been in the past year that we have developed the technologies to be able to distinguish between the two.
N. Ostrom: So you now have very reliable testing that will distinguish between Variant A and Variant B?
K. Knox: Yes.
N. Ostrom: Is it antibody testing, or DNA testing?
K. Knox: It is antibody testing. You could do both, but we use antibody testing.
N. Ostrom: And you test blood? Or do you look only at tissues?
K. Knox: We do tissue biopsies. We look in the tissue itself. And it is very difficult for people to dismiss the idea of HHV6-A because, frankly, nobody knows what the epidemiology is, how many healthy people are infected, how it's transmitted, those kinds of things. We don't know. And there is a unique kind of collaboration between HHV-6A and HIV that HHV-6B does not have. HHV-6B does cause disease. It kills immunocompromised patients. It kills transplant patients. But, with respect to AIDS and HIV infection, we believe that the A variant is what is important, because it has this special interaction with HIV. And variant A is in all the AIDS patients. You don't find it, even in other immunocompromised patients, like bone marrow transplant patients. There is something special about the interaction of the two viruses, HIV and HHV-6A.
N. Ostrom: Do you think they might have evolved together?
K. Knox: Actually, that is a very interesting thing to think about. Yes, I think that they have evolved together, and I think they really like hanging out together. There seems to be a selective advantage to the two viruses being in close proximity-and the tat protein of HIV is something HHV-6A seems to like. There's something that HHV-6A makes as well that, in our laboratories, gets HIV really revved up. If there's an advantage, viruses evolve together. If selective pressures are put on them, they will respond to make their environment more compatible. Viruses want to make more of themselves. They don't destroy things on purpose, because it's actually not to their advantage. It wouldn't surprise me, in their natural histories, if HHV-6A and HIV evolved together, because there's such an enhancement of the two viruses when they're together. Although in vitro (laboratory) studies published over the last eight or ten years have suggested a synergy between HIV and HHV-6A, in vivo (in the body) evidence has been lacking. Finally, we have examined the tissue of HIV-infected patients and asked, why do all these people have HHV-6A replicating in their tissues when they're still healthy, and we can't even find it in other immunocompromised patients? It's a very provocative finding. There's also a study you'll find interesting, that was performed by Italian researcher Dario Diluca, published in the Journal of Clinical Microbiology, I think. Dario has also been doing HHV-6A and HIV research. What he just published last summer is a PCR study of HHV-6 in Chronic Fatigue Syndrome patients. The unique finding concerned HHV-6A. Whereas you can find it in the peripheral lymphocytes of about four percent of healthy people, you see it in 22 percent of Chronic Fatigue Syndrome patients. There's no difference in the levels of HHV-7 and HHV-6B in healthy people and CFS patients, but the A variant was seen at four percent in healthy people and 22 percent in CFS patients, which is very significant.
N. Ostrom: In their natural killer cell paper, Lusso and Gallo showed that HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. They identified the problem in both sets of patients, so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.
K. Knox: Yes, it's a very disregulating virus. Variant B is not benign, but variant A is especially destructive. This is not only when we look at tissues, but also in the test tube-variant A is especially destructive. Which antiviral drugs do you know have effectiveness against HHV6-A? We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. Actually, with foscarnet, we have treated specifically HHV-6A infections and seen very nice reversals of clinical syndromes. We don't always know which variant we're treating when we're treating HHV-6. Also, if you look in the literature, there are three major studies looking at acyclovir in AIDS patients. These were patients with CD4s of less than 150. There was one study in particular that I'm recollecting in which there were about 300 patients. They treated half with AZT alone, and half with AZT plus acyclovir. What they wanted to do was to look to see if acyclovir could suppress CMV reactivation. Well, what they found was that it had no effect on CMV infection, but there was a curious, significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone. There are three major studies in the literature like that, and the speculation as to why that is? They don't know. And they don't address it, because they haven't got a clue as to why it might be. Now, we have never treated HHV-6 infections with acyclovir, because the B variant of the virus is resistant, and that's usually the virus that we see in transplant patients. But in laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than ganciclovir, and if you're talking about treating healthy people in a clinical trial, you're looking for something that people can take orally. You don't want them to have to come in for IV infusions, and foscarnet would require that. So I would say that acyclovir and its analogs and ganciclovir would be very interesting.
N. Ostrom: So, what you have discovered should be viewed as good news?
K. Knox: Oh, I think it's tremendously good news. I think it offers the best hope that we've seen in 15 years of this epidemic. That's because it's the first new approach. And the difference is that we believe that actually what destroys the immune organs, the lymph nodes, is HHV-6A. It is not HIV. HIV keeps it going, and HHV-6A keeps goosing HIV, and together they keep secreting products that each other love. They stroke each other. And that's a hard team to break up. You can't do it just by targeting HIV.
N. Ostrom: Is there anything else you'd like people to know about your research?
K Knox: Now that we've made the distinction between the two HHV-6 viruses, A and B, we're really hoping that funding is loosened up and the abuses of how AIDS research has been managed by the government agencies, by NIH-certainly, we've been caught in that trap. I just hope that they loosen up soon enough that we don't have to abort our program. And it's getting pretty close. It's pretty close. http://www.chronicillnet.org/online/Knox.html


Truth to Power
New York Native 1980-1997
Available at Amazon in every country.




By the time you finish this eye-opening book you will question everything you have been told about Chronic Fatigue Syndrome and AIDS. In this powerfully written history you will find credible and disturbing evidence linking the two epidemics to one virus, HHV-6. You will wonder if HHV-6 is the real AIDS/CFS virus and whether the HIV theory of AIDS is one of the biggest mistakes ever made in medical science. This book will inspire an international debate about HHV-6 and Chronic Fatigue Syndrome.

*Truth to Power exposes the corrupt world of AIDS and Chronic Fatigue Syndrome research.

*Truth to Power reveals how the Centers for Disease Control has covered up a massive epidemic of Chronic Fatigue Syndrome and HHV-6, the virus that clearly is what is destroying the immune systems of CFS patients.

*Truth to Power explains why HHV-6 has become the biggest public health problem in the world.

*Truth to Power reveals how HHV-6 may threaten your health and the health of your family and friends.

*Truth to Power uncovers the terrifying possibility that the virus HHV-6 is also infecting the pets of people with Chronic Fatigue Syndrome.

*Truth to Power presents compelling evidence that HHV-6 originated in pigs.

*Truth to Power shows you how political American science has become and why so many honest whistleblowers have been silenced.

Charles Ortleb’s Truth to Power takes you inside the New York Native, one of the most unique and consequential newspapers of the twentieth century. Shortly after starting his small gay New York City newspaper in late 1980, one of the biggest scientific and political stories of our time fell into his lap in the form of the AIDS and Chronic Fatigue Syndrome epidemic. What he did with that story has secured his newspaper’s place in history. Under his guidance, a succession of intrepid journalists did some of their greatest work uncovering the crucial facts about the labyrinthine epidemic.

Ortleb made the decision to follow the facts wherever they led. Charles Ortleb’s Truth to Power takes you inside the New York Native, one of the most unique and consequential newspapers of the twentieth century. Shortly after starting his small gay New York City newspaper in late 1980, one of the biggest scientific and political stories of our time fell into his lap in the form of the AIDS and Chronic Fatigue Syndrome epidemic. What he did with that story has secured his newspaper’s place in history. Under his guidance, a succession of intrepid journalists did some of their greatest work uncovering the crucial facts about the labyrinthine epidemic.

Ortleb made the decision to follow the facts wherever they led. As a result of the New York Native’s uncompromising investigative reporting, many powerful toes were stepped on. For years the medical and political establishment did everything they could to discredit New York Native and put it out of business. But Ortleb stood his ground for as long as possible and as a result the world now can have a clear understanding of the relationship of AIDS, Chronic Fatigue Syndrome, and HHV-6, the transmissible virus that now threatens everyone on this planet.

Anyone who has wondered why the medical establishment will not tell the truth about the Chronic Fatigue Syndrome epidemic will find the disturbing answer in Truth to Power.
What makes Ortleb so unusual is that not only did he have the natural instincts of a journalist, editor and publisher, but he was also a poet, a fiction writer and a budding political philosopher. Truth to Power is not just a compelling work of journalism and history, but also a major contribution to the intellectual life of our time.

Truth to Power is a 466-page book published by Rubicon Media.

Truth to Power is available on Amazon in both print and Kindle formats.  Also Kindle Unlimited.
Ask for it at your local independent bookstore.


HHV-6 and the Promise of Ampligen

This experimental drug not only stops HHV-6, it helps AIDS and CFS patients function.

Written by Neenyah Ostrom, first published in: New York Native, issue #663, January 1, 1996

During 1995, a series of extremely disturbing facts were revealed about the damage Human Herpes Virus 6 (HHV-6) is able to inflict. The virus was linked to the brain and nervous system damage seen in Multiple Sclerosis; scientists warned that HHV-6 is a dangerous contaminant of the blood supply, which is not screened for its presence, and is therefore probably being transmitted via transfusion; HHV-6 was found to be the most common infection in AIDS patients, rather than CMV as was previously assumed; it was implicated as a cause of the blinding AIDS retinitis; Italian research linked HHV-6 (Variant A) not only to AIDS and Chronic Fatigue Syndrome, but also to AIDS-associated Kaposi's sarcoma; and, perhaps most importantly, HHV-6 has been shown to be present in the lymph nodes of AIDS patients right from the beginning of their disease.
All of this has resulted in a growing number of scientists who routinely refer to HHV-6 as the "AIDS co-factor."
All of this sounds pretty grim. But there is also good news to report from 1995's scientific endeavors: There is a non-toxic, experimental drug that appears to be able to stop the virus cold in its tracks. The drug is Ampligen, a special form of RNA (the sister molecule to DNA, of which most viruses are composed); it interferes with HHV-6's ability to grow.
The bad news is that the seemingly effective and non-toxic Ampligen, for some impossible-to-understand reason, has yet to be approved by the Food and Drug Administration.
In clinical trials, Ampligen not only inhibits the growth of HHV-6 in tissue culture, but also appears to produce long-term improvement in patients with CFS-who are known to have active HHV-6 infections.
Two recent studies demonstrating Ampligen's effectiveness against HHV-6, performed by some of the leading researchers in the field of the virology of HHV-6 and the clinical treatment of CFS, have added significant ammunition to arguments that Ampligen should be approved by the FDA immediately.
Dharam V. Ablashi was lead author on the scientific report, published in the journal in vivo, which showed that Ampligen inhibited HHV-6 from growing in cells in tissue culture. In addition to other collaborators, well-established CFS researchers Robert Suhadolnik and Anthony Komaroff were investigators in this study.1
Ablashi and colleagues began by pointing out that, while it is believed most people are infected with HHV-6, "many different strains of the virus, comprising of two variants (the A and B variants), with different biologic properties, have been identified." And while HHV-6 has been associated with the generally-mild childhood illness roseola, active HHV-6 infection has also been reported in a number of conditions "known or suspected to be associated with immunological dysfunction." That list, according to Ablashi and colleagues, includes AIDS, Hodgkin's disease (lymphoma), autoimmune disorders like lupus, graft-versus-host disease, and Chronic Fatigue Syndrome.2
HHV-6's possible role in AIDS is particularly troubling, Ablashi and co-workers noted, since, "Like human immunodeficiency virus-1 (HIV-1), HHV-6 is tropic for CD4-positive T-cells; dual infection of CD4-positive cells with both HIV-1 and HHV-6 greatly enhances the rate of CD4-positive cell death." They continued, "Whether the synergistic cytopathic effects of HHV-6 and HIV-1 contributes to pathology or morbidity in HIV infected patients remains to be determined." In other words, does being infected with HHV-6 in addition to HIV indicate a worse prognosis than being infected with HIV alone? The experimental drug Ampligen, Ablashi and colleagues explain, is a mis-matched, double-stranded RNA that has "broad spectrum antiviral and immune modulating activity." They note that when used in combination with "a low dose of AZT," Ampligen "significantly reduced the cytopathic effect inducted by HIV-1" in cell cultures.
As Ablashi recently told the Native, however, giving AZT to an HHV-6 infected individual can, based on laboratory findings, have an extremely deleterious effect, since AZT not only increases the growth of the virus, but increases its cell-killing ability. (See Native #662, December 25, 1995, for the complete Ablashi interview.) Ampligen has also shown a positive effect on the clinical conditions of CFS and AIDS patients, these investigators point out. In particular, a long-term trial of Ampligen treatment of CFS patients resulted in "improved performance on exercise testing as well as improved quality of life, compared to those using a placebo." Therefore, "Since HHV-6 reactivation is frequently seen in CFS infection and since Ampligen treatment seemed to produce a clinical benefit in patients with CFS, we conducted in vitro [laboratory] studies to determine whether Ampligen had antiviral effects against HHV-6."
Cells infected with the GS strain of variant A HHV-6-the type most commonly detected in patients with CFS, AIDS, and other immunocompromised conditions-were treated with Ampligen while being grown in tissue culture, before and after being infected with HHV-6. Cells that were pretreated with Ampligen before infection with HHV-6 showed "substantial inhibition of virus replication, ranging from 45.7-78.3 percent."
A second variation of the experiment was the most successful: When cells were both pre-treated with Ampligen before HHV-6 infection, and then grown in culture with Ampligen present, as well, "inhibition of virus replication was nearly complete," Ablashi and co-workers reported.
In a third variation of the experiment, cells were not pretreated with Ampligen, but treated only at the time of viral infection; no Ampligen was added thereafter to the cultures. Even under these conditions, there was inhibition of viral replication, ranging from 45.7 to 89.1 percent.
The fourth permutation in this series of experiments was the also quite successful: When the cells were not pre-treated but were treated continuously with Ampligen after HHV-6 infection, there was a "dose related inhibition of virus replication, ranging from 95.5-91.3 percent at three different concentrations (50, 100, and 200 micrograms/milliliter)," Ablashi and colleagues report. A concentration of only ten micrograms/milliliter was not enough to inhibit HHV-6 infection, they found.
Perhaps the best news in this study is that inhibition of HHV-6 with Ampligen resulted in absolutely no toxicity to the cells; they remained "90 percent viable," i.e., alive.3 This study indicates that Ampligen appears not only to stop replication of the virus, but also to stop HHV-6 from maturing once it is in the cell.
But do those effects, in the lab, translate into clinical improvement when people with active HHV-6 infections are treated with Ampligen? In 1995, a study was published that showed long-term improvement in patients with Chronic Fatigue Syndrome who were treated with Ampligen. Ablashi was an investigator in this study, as were Ampligen co-inventor William Carter, CFS researchers Daniel Peterson, David R. Strayer, Robert J. Suhadolnik, Sheila Bastien, HHV-6 researcher Berch Henry, and others.4
The answer to the question of whether Ampligen improved the health of CFS patients, who are known to have active HHV-6 infections, was yes. Improvement was noted in patients' Karnofsky Performance Scale (KPS), a measure of ability to perform daily activities like taking care of oneself; memory and IQ improved; exercise tolerance was increased; and there was a measurable reduction of HHV-6 activity.
The Strayer paper reported not only these marked improvements in CFS patients treated with Ampligen, but that they were sustained over the long term.
Fifteen CFS patients, all of whom met the Centers for Disease Control criteria for CFS, participated in the experiment. Their mean age was 44, and 73 percent were women. These patients had been sick for an average of 33 months. "All 15 patients were functionally impaired by their illness as evidenced by their mean baseline Karnofsky Performance Score of 47 (range 20-60)," Strayer and colleagues reported. A KPS score of 100 is considered normally functional. There were two dose regimens administered to the study participants. Initially, they received 200 milligram of Ampligen intravenously twice a week "for variable periods of time"; then, the dosage was increased to 400 milligrams twice a week. Some patients' doses were increased to 400 milligrams three times a week.
Patients were monitored for active Human Herpes Virus 6 infection by blood cultures, which were "observed periodically for the formation of giant cells characteristic of herpesvirus infection," according to Strayer et al. HHV-6 itself was found in those giant cells, and the percentage of those cells infected with Variant A HHV-6 (the GS strain) was determined.
Some patients had more than ten percent "giant cells" in their cultured blood cells, scored as "two"; those with between 0 percent and ten percent scored as "one"; and those with no giant cells scored as "zero."5
No patient in the study dropped out because of toxicity from the drug. At the beginning of Ampligen therapy, patients reported an increase in flu-like symptoms (muscle and headaches), but those symptoms "typically abated" as treatment continued.
"There were no clinically significant alterations of coagulation, blood chemistry values, white blood counts, or liver and renal function test values throughout the course of this study," Strayer and colleagues reported. "Only two adverse events, one case each of feeling lightheaded and facial flushing, were reported as definitely related to Ampligen. There were no severe adverse events attributed to Ampligen." One patient became anemic because of the amount of blood drawn for testing, and was treated with an iron supplement. There were also changes in laboratory blood test values-red blood cell count, hemoglobin, numbers of different types of lymphocytes and platelets-noted during this study. Blood clotting remained normal, as did urinalysis.
Perhaps the most striking improvement was measured by the Karnofsky Performance score (KPS), as Strayer and co-workers explained: "Patients entering the study were significantly incapacitated, with a mean Karnofsky performance score (KPS) of 47. At a KPS level of 40-50 an individual is significantly disabled and requires special care or considerable assistance to perform normal activities of daily living. Self-care is limited and 50 percent or more of the individual's's waking hours are spent confined to bed and/or chair. The average score improved to 67 after 12 weeks of Ampligen therapy. A KPS score of 60-70 describes an individual able to care for most needs with no or only occasional assistance, but unable to carry out any work activities.
"KPS showed sustained improvements through 60 weeks, reaching 80 by 24 weeks and 85 by 60 weeks. An 80 KPS score describes a person capable of normal activity with effort. Some signs and symptoms of disease are still present but no special care is required. The [statistical analysis performed] strongly suggested that the continued increase in KPS during the first 24 weeks of Ampligen therapy was statistically significant."6
Ampligen also reduced the presence of the giant cells indicative of HHV-6 infection. All 14 patients were positive for giant cells before Ampligen treatment. The number of such cells increased during Ampligen treatment in 50 percent of the patients at eight weeks, and in 77 percent at 16 weeks. Four of the patients actually became culture-negative for HHV-6 during Ampligen treatment. In other words: Ampligen stops HHV-6.
In fact, this not-yet-approved, non-toxic drug appears to inhibit the growth of the "AIDS cofactor" completely.
In addition to the other clinical improvements noted during Ampligen treatment, cognitive functioning also increased. Memory scores increased as much as 23 to 45 percent, as did IQ scores.
Only two of the patients in the study failed to experience all of these improvements in clinical status, for unknown reasons. The clinical effects of Ampligen, like its ability to inhibit HHV-6's growth, appeared to be dose-dependent; the most dramatic improvements in daily functioning, Strayer and co-authors point out, occurred after Ampligen dosage was increased to 400 milligrams.
Strayer and colleagues speculate that these clinical improvements could be associated with Ampligen's inhibition of HHV-6.
"Reduced ability to obtain giant cells in short term culture of blood mononuclear cells was noted during Ampligen treatment," they reported. "In eight cases, giant cells were shown to express HHV-6, utilizing specific monoclonal antibodies. This could have resulted from a restoration of normal lymphokine balance, from direct inhibition of virus replication, or from elimination of HHV-6 expressive cells by immune mechanisms. Giant cell formation in this system is associated with HHV-6 infection, but it is not known whether HHV-6 expression or giant cell formation contributes to CFS symptomatology. However, recent studies show that Ampligen can inhibit in vitro replication of HHV-6...."
Why has this seemingly safe, effective drug not been approved by the FDA?
Is it because a treatment that proves effective for both CFS and AIDS would highlight the connection between the two syndromes?

References

  1. Ablashi, D.V. et al.; "Ampligen Inhibits Human Herpesvirus-6 in Vitro"; in vivo 8:587, 1994.
  2. Ibid.
  3. Ablashi et al., op cit.
  4. Strayer, David R. et al.; "Long Term Improvements in Patients With Chronic Fatigue Syndrome Treated With Ampligen"; Journal of Chronic Fatigue Syndrome 1(1):35, 1995.
  5. Ibid.
  6. Strayer et al., op cit


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.


Important and provocative books about HHV-6 and the epidemics it may be causing available from Amazon in print editions or on Kindle:


The Virus Within by Nicholas Regush (Print Edition)



What Really Killed Gilda Radner? Frontline Reports on the Chronic Fatigue Syndrome Epidemic by Neenyah Ostrom (Print Edition)

50 Things You Should Know About the Chronic Fatigue Syndrome Epidemic by Neenyah Ostrom (Print Edition)

America's Biggest Cover-Up: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic And Its Link to AIDS by Neenyah Ostrom (Print Edition)



HHV-6 and Thymocyte Depletion

Human Herpesvirus 6 (HHV-6) Causes Severe Thymocyte Depletion in SCID-hu Thy/Liv Mice

Human herpesvirus 6 (HHV-6) is a potentially immunosuppressive agent that may act as a cofactor in the progression of AIDS. Here, we describe the first small animal model of HHV-6 infection. HHV-6 subgroup A, strain GS, efficiently infected the human thymic tissue implanted in SCID-hu Thy/Liv mice, leading to the destruction of the graft. Viral DNA was detected in Thy/Liv implants by quantitative polymerase chain reaction (PCR) as early as 4 d after inoculation and peaked at day 14. The productive nature of the infection was confirmed by electron microscopy and immunohistochemical staining. Atypical thymocytes with prominent nuclear inclusions were detected by histopathology. HHV-6 replication was associated with severe, progressive thymocyte depletion involving all major cellular subsets. However, intrathymic T progenitor cells (ITTPs) appeared to be more severely depleted than the other subpopulations, and a preferred tropism of HHV-6 for ITTPs was demonstrated by quantitative PCR on purified thymocyte subsets. These findings suggest that thymocyte depletion by HHV-6 may be due to infection and destruction of these immature T cell precursors. Similar results were obtained with strain PL-1, a primary isolate belonging to subgroup B. The severity of the lesions observed in this animal model underscores the possibility that HHV-6 may indeed be immunosuppressive in humans. --By Alberto Gobbi, Cheryl A. Stoddart,Dagger Mauro S. Malnati, Giuseppe Locatelli, Fabio Santoro, Nancy W. Abbey, Christopher Bare, Dagger Valerie Linquist-Stepps, Dagger Mary Beth Moreno, Dagger Brian G. Herndier,§ Paolo Lusso, and Joseph M. McCune, J. Exp. Med., Volume 189, Number 12, June 21, 1999 1953-1960

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.


Saturday, June 29, 2013

Virologic and Immunologic Evidence Supporting an Association between HHV-6 and Hashimoto's Thyroiditis

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002951



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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New York Native Chapters 2

New York Native Chapters 3

Final New York Native Chapter

Audible CFS book

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