Bulletins from The Coordinating Committee of The International HHV-6 Protest and Teach-in At Harvard (November 9-11, 2015)

- September 22, 2015

Bulletin #66

When will Ta-Nehisi Coates realize that the CDC's fraudulent AIDS paradigm has resulted in mass epidemiological incarceration of the Black community and a new Tuskegee Syphilis kind of experiment?

http://www.theatlantic.com/magazine/archive/2015/10/the-black-family-in-the-age-of-mass-incarceration/403246/

Bulletin #65

Interview with Konnie Knox, the scientist who should receive a Nobel Prize for her work on HHV-6

Dr. Konstance Knox, Chief Executive Officer Dr. Knox was a co-founder of Wisconsin Viral Research Group and Viracor, infectious disease diagnostic laboratories specializing in the diagnosis of viral infections in patients with compromised systems including patients with HIV/AIDS and bone marrow/stem cell transplant and solid organ transplant recipients. Dr. Knox earned her PhD in experimental pathology from the Medical College of Wisconsin and completed her post-doctoral training in translational medicine in the Immunotherapy/Gene Therapy Division of the Cancer Program at St. Luke's Medical Center in Milwaukee, Wisconsin. Dr. Knox's research interests have focused on the role of persistent viral and prion infections in chronic diseases of animals and humans, especially as they relate to diseases of the central nervous system (CNS). She served as a Special Scientific Reviewer for the Department of Defense National Prion Research Program, and for the National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland. Dr. Knox is the author and co-author on 41 peer reviewed scientific publications. Currently she serves on the Scientific Advisory Board on the Chronic Fatigue Syndrome Association of Wisconsin, and is Chair of the Scientific Advisory Board for Simmaron Research Foundation, Incline Village, Nevada.

Earth to Paris: Wake up!

Should Luc "Madoff" Montagnier, stop living the high life off of the HIV fraud Pnzie scheme and turn his Nobel Prize over to Konnie Knox and admit that HHV-6 is the real culprit?

The Virus Within by Nicholas Regush

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. --Nicholas Regush The Virus Within page 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 The Virus Within page 54

Knox was fascinated by how HHV-6, like HIV, attacked T-4 lymphocytes, monocytes and macrophages. --Nicholas Regush The Virus Within Page 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 the 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. --Nicholas Regush The Virus Within Page 83

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. --Nicholas Regush The Virus Within Page 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. --Nicholas Regush The Virus Within Page 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 The Virus WithinPage 87

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. --Nicholas Regush The Virus Within Page 89

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-infected AIDS patients, 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 would 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. --Nicholas Regush The Virus Within Page 95

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. --Nicholas Regush The Virus Within Page 97

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. --Nicholas Regush 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. --Nicholas Regush The Virus Within Page 101

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. --Nicholas Regush The Virus Within Page 102
Science is not a democracy, Knox was learning. Science sometimes punishes people for pursuing the truth. --Nicholas Regush The Virus Within Page 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. --Nicholas Regush The Virus Within page 114

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. --Nicholas Regush The Virus Within Page 183

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. --Nicholas Regush The Virus Within page 223

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? --Nicholas Regush The Virus Within Page 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 The Virus WithinPage 225

HHV-6 Flashback: 1995

HHV-6 PETER JENNINGS REPORT ON ABC NEWS BREAKS THE NEWS OF A SECOND AIDS VIRUS TO THE NATION

On Dec. 7th, 1995, ABC News carried a nationwide televised broadcast on another virus that may be the cause of AIDS - HHV-6. Robert Gallo was quoted as saying that: “When you compare the two viruses (HIV and HHV-6), in a laboratory, the more destructive by far is HHV-6.” Peter Jennings said he had heard something about variant strains of the virus, but Gallo avoided answering him directly and repeated his reference to HHV-6, without indicating that variant A is the co-factor in AIDS. Robert Gallo knows more than he is saying publicly. Several researchers have published articles in medical journals that identified variant A as the virulent HHV-6 co-factor in AIDS.
In the ABC News interview, Virologist Konstance Knox, who works at the Medical College of Wisconsin, described the effects of HHV-6 infection in people: “It can kill people. It can cause fatal brain disease. It can cause fatal bone marrow destruction. It can cause fatal lung infection.” ABC News news reporter McKenzie told viewers that researchers now believe that HHV-6 “works together with HIV, by attacking the immune system, unleashes the HHV-6 to ravage the body.”

http://www.keephopealive.org/report10.html

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.
https://web.archive.org/web/20010204035700/http://www.chronicillnet.org/online/knox.html

Bulletin #64

Every French writer, intellectual, doctor, scientist and activist concerned about the integrity of the Pasteur Institute should read this:

The following was written by Kary Mullis for the introduction to the book "Inventing the AIDS Virus" by Peter H. Duesberg (Regnery Publishing, INC; Washington DC, 1996):

   In 1988 I was working as a consultant at Specialty Labs in Santa Monica, CA, setting up analytic routines for the Human Immunodeficiency Virus (HIV). I knew a lot about setting up analytic routines for anything with nucleic acids in it because I invented the Polymerase Chain Reaction. That's why they hired me.
   Acquired Immune Deficiency Syndrome (AIDS), on the other hand, was something I did not know a lot about. Thus, when I found myself writing a report on our progress and goals for the project, sponsored by the National Institutes of Health, I recognized that I did not know the scientific reference to support a statement I had just written: "HIV is the probable cause of AIDS."
   So I turned to the virologist at the next desk, a reliable and competent fellow, and asked him for the reference. He said I didn't need one. I disagreed. While it's true that certain scientific discoveries or techniques are so well established that their sources are no longer referenced in the contemporary literature, that didn't seem to be the case with the HIV/AIDS connection. It was totally remarkable to me that the individual who had discovered the cause of a deadly and as-yet-uncured disease would not be continually referenced in the scientific papers until that disease was cured and forgotten. But as I would soon learn, the name of that individual - who would surely be Nobel material - was on the tip of no one's tongue.
   Of course, this simple reference had to be out there somewhere. Otherwise, tens of thousands of public servants and esteemed scientists of many callings, trying to solve the tragic deaths of a large number of homosexual and/or intravenous (IV) drug-using men between the ages of twenty-five and forty, would not have allowed their research to settle into one narrow channel of investigation. Everyone wouldn't fish in the same pond unless it was well established that all the other ponds were empty. There had to be a published paper, or perhaps several of them, which taken together indicated that HIV was the probable cause of AIDS. There just had to be.
   I did computer searches, but came up with nothing. Of course, you can miss something important in computer searches by not putting in just the right key words. To be certain about a scientific issue, it's best to ask other scientists directly. That's one thing that scientific conferences in faraway places with nice beaches are for.
   I was going to a lot of meetings and conferences as part of my job. I got in the habit of approaching anyone who gave a talk about AIDS and asking him or her what reference I should quote for that increasingly problematic statement, "HIV is the probable cause of AIDS."
   After ten or fifteen meetings over a couple years, I was getting pretty upset when no one could cite the reference. I didn't like the ugly conclusion that was forming in my mind: The entire campaign against a disease increasingly regarded as a twentieth century Black Plague was based on a hypothesis whose origins no one could recall. That defied both scientific and common sense.
   Finally, I had an opportunity to question one of the giants in HIV and AIDS research, DL Luc Montagnier of the Pasteur Institute, when he gave a talk in San Diego. It would be the last time I would be able to ask my little question without showing anger, and I figured Montagnier would know the answer. So I asked him.
   With a look of condescending puzzlement, Montagnier said, "Why don't you quote the report from the Centers for Disease Control? "
   I replied, "It doesn't really address the issue of whether or not HIV is the probable cause of AIDS, does it?"
   "No," he admitted, no doubt wondering when I would just go away. He looked for support to the little circle of people around him, but they were all awaiting a more definitive response, like I was.
   "Why don't you quote the work on SIV [Simian Immunodeficiency Virus]?" the good doctor offered.
   "I read that too, DL Montagnier," I responded. "What happened to those monkeys didn't remind me of AIDS. Besides, that paper was just published only a couple of months ago. I'm looking for the original paper where somebody showed that HIV caused AIDS.
   This time, DL Montagnier's response was to walk quickly away to greet an acquaintance across the room.

http://www.duesberg.com/viewpoints/kintro.html

Bulletin #63

Bulletin #62

Bulletin #61

Letter from Congressman Jerrald Nadler to Secretary of Health and Human Services Donna E. Shalala, April 12, 1996:

Statement read by Congressman Nadler on the floor of the House of Representatives:

Bulletin #60

In a conversation about the role of HHV-6 in AIDS, Konnie Knox said it "sets the tempo of the disease and may be required to pathology and mortality."

Bulletin #59

Bulletin #58

Bulletin #57

Will Truvada be tomorrow's Risperdal?????

http://highline.huffingtonpost.com/miracleindustry/americas-most-admired-lawbreaker/chapter-3.html

Bulletin #56

Bulletin #55

Bulletin #54

LLewellyn King on British Official with Chronic Fatigue Syndrome, Senator Elizabeth Warren, and Senator Bill Cassidy

Bulletin #53

Bulletin #52

Bulletin #51

Bulletin #50

Another hint that Chronic Fatigue Syndrome is a subset of the HHV-6/AIDS epidemic?

Azithromycin in Chronic Fatigue Syndrome (CFS), an analysis of clinical data

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1562448/

" Certain bacterial respiratory diseases (such as pneumonia) are opportunistic infections. An opportunistic infection is an infection that occurs more frequently or is more severe in people with weakened immune systems—such as those infected with HIV—than in people with healthy immune systems.

Azithromycin can also be used 'off-label' to prevent and treat other opportunistic infections of HIV infection. 'Off-label' use refers to use of an FDA-approved medicine in a manner different from that described on the medicine label. Good medical practice and the best interests of a patient sometimes require that a medicine be used 'off-label.'"
https://aidsinfo.nih.gov/drugs/104/azithromycin/0/patient

Bulletin #49

Bulletin #48

The Larry Kramer of HHV-6 activism has been found!

Bulletin #47

One of the many films that should be shown to the students at Harvard during the International HHV-6 Protest and Teach-in

Bulletin #46

Mark Konlee on HHV-6

On Dec. 7th, 1995, ABC News carried a nationwide televised broadcast on another virus that may be the cause of AIDS - HHV-6. Robert Gallo was quoted as saying that: “When you compare the two viruses (HIV and HHV-6), in a laboratory, the more destructive by far is HHV-6.” Peter Jennings said he had heard something about variant strains of the virus, but Gallo avoided answering him directly and repeated his reference to HHV-6, without indicating that variant A is the co-factor in AIDS. Robert Gallo knows more than he is saying publicly. Several researchers have published articles in medical journals that identified variant A as the virulent HHV-6 co-factor in AIDS. In the ABC News interview, Virologist Konstance Knox, who works at the Medical College of Wisconsin, described the effects of HHV-6 infection in people: “It can kill people. It can cause fatal brain disease. It can cause fatal bone marrow destruction. It can cause fatal lung infection.” ABC News news reporter McKenzie told viewers that researchers now believe that HHV-6 “works together with HIV, by attacking the immune system, unleashes the HHV-6 to ravage the body.”
--Mark Konlee
http://www.keephopealive.org/report10.html

Bulletin #45

HHV-6 desperately needed a Larry Kramer.

And we found one!

Please post this on all social media
and help the message go viral!

Bulletin #44

The Last Lovers on Earth

There has never been a movie quite like this. Three thematically intertwined stories about gay characters on the edge build to an explosive conclusion. This irreverent independent film uses outrageous satire and zany humor to capture the heartbreaking disaster that "AIDS" has become. This entertaining and provocative film leaves you wondering what you can still believe is true about "AIDS."

Available at Amazon

Bulletin #43

Bulletin #42

If HHV-6 is the cause of Alzheimer's (among other things), of course Alzheimer's is transmissible. Duh!
http://www.independent.co.uk/life-style/health-and-families/health-news/alzheimers-disease-may-be-infectious-study-suggests-10493032.html

Researchers from the University of Bologna, Italy, have published data suggesting that HHV-6 and EBV are associated with Alzheimer’s Disease (AD) in elderly persons.
http://hhv-6foundation.org/news/hhv-6-and-ebv-identified-as-risk-factors-in-alzheimers-disease

Bulletin #41

BREAKING NEWS

The Horror of African Swine Fever in Eastern Europe

"The disease is spreading out in all directions."

"This scourge is becoming ingrained in Eastern Europe."

http://www.thepigsite.com/swinenews/40320/the-horror-of-african-swine-fever-in-eastern-europe/

Bulletin #40

"The CDC [Centers for Disease Control and Prevention], for example, has made some pretty big mistakes in handling CFS, mistakes that continue to hurt patients."

-- Julie Rehmeyer

http://www.senseaboutscienceusa.org/epistemically-challenged-julie-rehmeyer/

Bulletin #39

Doesn't Montoya know how serious HHV-6 is? And it's obvious multisystemic role in AIDS?

Bulletin #38

How HHV-6 Could Cause AIDS and Cancer

GP96 Interacts with HHV-6 during Viral Entry and Directs It for Cellular Degradation

http://www.ncbi.nlm.nih.gov/pubmed/25470779

gp96—The immune system's Swiss army knife

"The cellular heat shock protein gp96 is turning out to be a rather versatile molecule. It has long been known for its ability to induce immunity against antigens from the cell from which it came."

http://www.nature.com/ni/journal/v1/n2/full/ni0800_100.html

Bulletin #37

HHV-6 activism needs a Lily Tomlin!

Bulletin #36

Bulletin #35

Does Michael Wolz know that HHV-6, HHV-7 and HHV-8 may really be pig viruses? Is that why they affect the skin the way they do? What about the relationship between HHV-8 and African Swine Fever in Sardinia? What is the relationship between HHV-6/7 and Porcine lymphotropic herpesviruses 1 and 2?

Bulletin #34

Bulletin #33

Stuart Murdoch of Belle and Sebastian ME/CFS Interview in L.A.

Belle & Sebastian
please come to
The International HHV-6 Protest

Bulletin #32

Bulletin #31

HHV-6 Needs a Larry Kramer!

Bulletin #30

Is this what is happening to Generation HHV-6?

The impact of chronic fatigue syndrome on cognitive functioning in adolescents.

http://www.ncbi.nlm.nih.gov/pubmed/26334394

Bulletin #29

Bulletin #28

The presence of roseola virus in chromosomes triples the risk of angina

http://medicalxpress.com/news/2015-06-presence-roseola-virus-chromosomes-triples.html

Bulletin #27

Bulletin #26

Bulletin #25

Forgotten Plague producer and co-director Ryan Prior announces the production's plans to partner with Tugg, a revolutionary new company giving documentaries a unique opportunity to stage screenings all across the world.

More info at: http://www.forgottenplague.com/

Bulletin #24

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Bulletin #21

One publication dared to tell the truth

about HHV-6 in 1995.

The New York Native 1980-1997

A 20th Century Newspaper of Firsts

1. First newspaper to break the story of AIDS.

2. First newspaper to make AIDS its signature story.

3. First newspaper the Centers for Disease Control leaked news of the discovery of what the institution thought was the "cause of AIDS.

4. First newspaper to do an in-depth interview with Robert Gallo.

5. The first newspaper to raise questions on a regular basis about Robert Gallo's so-called "discovery," and to provide thorough coverage of the Gallo scandal.

6. The first newspaper to cover the scientists who found holes in the HIV theory of AIDS and who dared to criticize the powerful AIDS establishment.

7. The first newspaper to publish investigative reporting on AZT.

8. The first newspaper to provide regular coverage of HHV-6, the "other AIDS virus."

9. The first newspaper to have a full time reporter covering the chronic fatigue syndrome epidemic.

10. The first newspaper to do investigative reporting on the intertwined nature of AIDS and chronic fatigue syndrome.

Bulletin #20

Bulletin #19

Is this 1988 paper on HHV-6 and African Swine Fever Virus by Dharam Ablashi legimate or should it be retracted?

http://www.researchgate.net/publication/19958785_HBLV_is_not_ASFV

Bulletin #18

Bulletin #17

Oh no! The truth about HHV-6, AIDS and Chronic Fatigue Syndrome might come out of the closet!

"The majority of the new grant will fund research in these overlapping research areas—including chronic fatigue syndrome, heart disease and others. It will also continue to fund Calabrese and Lederman's research on HIV/AIDS."

http://www.cleveland.com/healthfit/index.ssf/2015/08/cleveland_hivaids_research_duo.html

Bulletin #16

Bulletin #15

Ian Lipkin receives $765,000 to Continue

HHV-6 Cover-up

http://www.cortjohnson.org/blog/2015/08/23/lipkin-nih-grants-chronic-fatigue-syndrome-2015/

Bulletin #14

A Dutch male ballet dancer with quite severe M.E. talks about his illness.
https://www.youtube.com/watch?v=P3Kg1H-cfnI&feature=youtu.be

Bulletin #13

The HHV-6 Follies

Cartoons from HHV-6 University

Bulletin #12

For three days in November, Harvard University will become HHV-6 University

Statements to be discussed at the HHV-6 Teach-ins at Harvard on November 9-11, 2015

"The basic thing you should know is that nearly all ME/CFIDS patients have a virus called HHV-6A and inside that is a retrovirus that one researcher has named the JHK virus." Editor of The National Forum

"So, I believe human herpesvirus-6 is a factor in AIDS progression." --Robert Gallo http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html

"As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV." --Konnie Knox http://www.chronicillnet.org/online/Knox.html

"It seems wherever HHV-6 is going, you're bound to bump into HIV. It's like a cohabitation." --Robert Gallo http://www.aegis.com/news/newsday/1992/ND920206.html

"All the evidence now available indicates that of the two viruses, HIV and HHV-6A, the most destructive by far is HHV-6A which has all the characteristics of African Swine Fever virus." --Mark Konlee

"The evidence that CFS may reflect human infection with mouse retroviruses (XMRV and the polytropic murine leukemia viruses (MLVs) has been seriously challenged. However this does not alter the evidence of neurological dysfunction in CFS, and it does not have a bearing on evidence linking CFS with other neurotropic viruses--particularly human herpesvirus six and enteroviruses." --Anthony Komaroff, Nature Reviews Neuroscience, advance online publication, Published online 27 July 2011

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 The Virus Within page 54

Knox was fascinated by how HHV-6, like HIV, attacked T-4 lymphocytes, monocytes and macrophages. --Nicholas Regush The Virus Within Page 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. --Nicholas Regush The Virus Within Page 83

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. --Nicholas Regush The Virus Within Page 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. --Nicholas Regush The Virus Within Page 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. The Virus Within Page 87

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. --Nicholas Regush The Virus Within Page 89

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-infected AIDS patients, 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. --Nicholas Regush The Virus Within Page 95

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. --Nicholas Regush The Virus Within Page 97

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. --Nicholas Regush 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. --Nicholas Regush The Virus Within Page 101

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. --Nicholas Regush The Virus Within Page 102

Science is not a democracy, Knox was learning. Science sometimes punishes people for pursuing the truth. --Nicholas Regush The Virus Within Page 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. --Nicholas Regush The Virus Within page 114

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. --Nicholas Regush The Virus Within Page 183

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. --Nicholas Regush The Virus Within page 223

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? --Nicholas Regush The Virus Within Page 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 The Virus Within Page 225

Bulletin #11

John Beldekas, Gallo, Ablashi and HHV-6

In August, 1986, John Beldekas was invited to go to the NCI and present his findings on the link between ASFV [African Swine Fever virus] and AIDS, which he did. Beldekas gave samples of all his lab work to Gallo. Later, the government asked Beldekas to turn over all his reagents and lab work to the government, which he did. Beldekas had found ASFV presence in nine of 21 AIDS patients using two standard procedures. At the meeting, Gallo was reported saying: “we know it is not ASFV.” How could Gallo know this as he hadn’t done any of his own tests to look for ASFV?

Two months later, Gallo published an article in Science (Oct 31, 1986) that he discovered a new possible co-factor in AIDS, a virus he called Human B Cell Lymphotropic Virus which he named HBLV. Like ASFV, HBLV infected B cells and also lived in macrophages. Did Gallo steal Beldekas’s ASF virus he found in AIDS patients and rename it HBLV? Later on, when Gallo found that HBLV could also infect other immune cells, he changed the name of HBLV to HHV-6. Eventually, Gallo identified his HBLV as the variant A strain of HHV-6 and called it a human herpesvirus.

--Mark Konlee

http://www.keephopealive.org/report10.html

Bulletin #10

Tony Fauci, you don't think the value of women's labor worth fighting for? Rather see country pay billions in SSDI endlessly? Ur going down.
— Hillary Johnson (@oslersweb) August 21, 2015

Bulletin #9

Bulletin #8

Bulletin #7

Lobbyists seek new funds for chronic fatigue syndrome research

http://news.sciencemag.org/biology/2015/08/lobbyists-seek-250-million-new-funds-chronic-fatigue-syndrome-research

Bulletin #6
The Coordinating Committee of the International HHV-6 Protests and Teach in at Harvard urges all attendees of the conference and protest (as well as their supporters) to sign the Harvard Declaration of the HHV-6 Rights of Man.

The Harvard Declaration of the
HHV-6 Rights of Man

We scientists and citizens of conscience demand that the following rights be upheld by governments and scientists s all over the world:

1. The right not to be lied to about the role of HHV-6 in AIDS.

2. The right not to be lied to about the role of HHV-6 in Chronic Fatigue Syndrome.

3. The right not to be lied to about the role of HHV-6 in Autism.

4.The right not to be lied to about the role of HHV-6 in Multiple Sclerosis.

5. The right not to be lied to about the role of HHV-6 in Brain Cancer.

6. The right not to be lied to about the role of HHV-6 in Heart Disease.

7. The right not to be lied to about the role of HHV-6 in Encephalitis.

8. The right not to be lied to about the role of HHV-6 in Cognitive Dysfunction.

9. The right not to be lied to about the role of HHV-6 in Drug Hypersensitivity Syndrome.

10. The right not to be lied to about the role of HHV-6 in Bone Marrow Suppression.

11. The right not to be lied to about the role of HHV-6 in Lymphadenopathy.

12. The right not to be lied to about the role of HHV-6 in Colitis.

13. The right not to be lied to about the role of HHV-6 in Endocrine Disorders.

14. The right not to be lied to about the role of HHV-6 in Liver Disease.

15. The right not to be lied to about the role of HHV-6 in Hodgkin's Lymphoma.

16. The right not to be lied to about the role of HHV-6 in Glioma.

17. The right not to be lied to about the role of HHV-6 in Cervical Cancer.

18. The right not to be lied to about the role of HHV-6 in Hypogammaglobulinemia.

19. The right not to be lied to about the role of HHV-6 in Optic Neuritis.

20. The right not to be lied to about the role of HHV-6 in Microangiopathy.

21. The right not to be lied to about the role of HHV-6 in Mononucleosis.

22. The right not to be lied to about the role of HHV-6 in Uveitis.

23. The right not to be lied to about the role of HHV-6 in Stevens-Johnson Syndrome.

24. The right not to be lied to about the role of HHV-6 in Rhomboencephalitis.

25. The right not to be lied to about the role of HHV-6 in Limbic Encephalitis.

26. The right not to be lied to about the role of HHV-6 in Encephalomyelitis

27. The right not to be lied to about the role of HHV-6 in Pneumonitis.

28. The right not to be lied to about the role of HHV-6 in GVHD.

29. The right not to be lied to about the role of HHV-6 in Ideopathic Pneumonia.

30. The right not to be lied to about the role of HHV-6 in Pediatric Adrenocortical Tumors

31. The right not to be lied to about the role of HHV-6 in the reactivation of endogenous retroviruses.

32. The right not to be lied to about the impact of HHV-6 on T-Cells.

33. The right not to be lied to about the impact of HHV-6 on B-Cells

34. The right not to be lied to about the impact of HHV-6 on Epithelial Cells.

35. The right not to be lied to about the the impact of HHV-6 on Natural Killer Cells.

35. The right not to be lied to about the the impact of HHV-6 on Dendritic Cells.

36. The right not to be lied to about the the impact of HHV-6 infection of the brain.

37. The right not to be lied to about the the impact of HHV-6 infection of the liver.

38. The right not to lied to about the ability of HHV-6 to affect cytokine production.

39. The right not to be lied to about the ability of HHV-6 to affect Aortic and Heart Microvascular Endothelial cells.

40. The right not to be lied to about the role of an HHV-6 cover-up in a massive HIV Fraud Ponzi Scheme that in a number of ways resembles the Tuskegee Syphilis Experiment and Nazi medicine.

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.

It's time to recognize that HHV-6A, HHV-6B, HHV-7 and HHV-8 all belong in a viral category of their own. Leaving them in the herpesvirus family trivializes their impact on public health and turns them into some kind of biomedical joke.

Here are the proposed new names for HHV-6A, HHV-6B, HHV-7 and HHV-8:

The AIDS Spectrum Viruses

HHV-6A should be called AIDS Spectrum Virus 1 (ARV-1)

HHV-6B should be called AIDS Spectrum Virus 2 (ARV-2)

HHV-7 should be called AIDS Spectrum Virus 3 (ARV-3)

HHV-8 should be called AIDS Spectrum Virus 4 (ARV-4)

The name of Chronic Fatigue Syndrome should be changed to AIDS Spectrum Virus Syndrome
(AIDS Virus Syndrome or ASVS.)

Bulletin #5

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if these Australian scientists had been listened to:
http://www.virusmyth.com/aids/perthgroup/

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this doctor had been had been listened to.
http://www.virusmyth.com/aids/index/mirwin.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this British Journalist had been had been listened to.
http://www.virusmyth.com/aids/index/nhodgkinson.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Director of the Department of Virology had been had been listened to.
http://www.virusmyth.com/aids/index/bgriffin.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this specialist in internal medicine had been had been listened to.
http://www.virusmyth.com/aids/index/rgiraldo.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Professor of Law had been listened to.
http://www.virusmyth.com/aids/index/pjohnson.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this New York City journalist had been listened to.

http://www.virusmyth.com/aids/index/cfarber.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Australian mathematician had been listened to.
http://www.virusmyth.com/aids/index/mcradock.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzie scheme and HHV-6 cover-up might have been exposed years ago if this Editor-at-Large for Nature Biotechnology and Research Editor of Bio/Technology had been listened to.
http://www.virusmyth.com/aids/index/hbialy.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Miami journalist had been listened to.
http://www.virusmyth.com/aids/hiv/ebhiv.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Harvard scholar had been listened to.
http://www.virusmyth.com/aids/index/jlauritsen.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Nobel Prize winner had been listened to.
http://www.virusmyth.com/aids/index/kmullis.htm

The Montagnier-Agut HIV Fraud and Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this Professor of Mathematics at Yale University had been listened to.
http://www.virusmyth.com/aids/index/slang.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this pathologist and microscoptist had been listened to.
http://www.virusmyth.com/aids/index/edharven.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this mathematician had been listened to.
http://aidswiki.net/index.php/Rebecca_Culshaw

www.scientificexploration.org/journal/reviews/reviews_21_2_bauer.pdf

http://www.amazon.com/Science-Sold-Out-Really-Cause/dp/1556436424

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this scientist had been listened to.
http://www.virusmyth.com/aids/index/pduesberg.htm

The Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi scheme and HHV-6 cover-up might have been exposed years ago if this AIDS activist had been had been listened to.
http://www.virusmyth.com/aids/index/chjohnson.htm

Bulletin #4
The Coordinating Committee of The International HHV-6 Protest and Teach-in At Harvard (November 9-11, 2015) urges artists all over the world to begin creating graphics that help expose the Gallo-Montagnier-Agut-Ablashi HIV Fraud Ponzi Scheme and HHV-6 Cover-up.

It time to use art to confront propaganda with truth.

Bulletin #3

The Coordinating Committee of The International HHV-6 Protest and Teach-in At Harvard (November 9-11, 2015) has issued the following cartoon to the students, scientists and protesters who will be attending the international HHV-6 protest and teach-in at Harvard.

Bulletin #2

The Coordinating Committee of The International HHV-6 Protest and Teach-in At Harvard (November 9-11, 2015) urges Harvard University to screen Ryan Prior's documentary, Forgotten Plague, during the HHV-6 Teach-in At Harvard (November 9-11).

Bulletin #1

Phoenix Rising has created an Action Alert to bump a thread on HBO's forums for "Last Week Tonight with John Oliver" about funding for ME/CFS:

http://talk.hbo.com/t5/Last-Week-To...nding-for-CFS-down-to-zero/m-p/496181#U496181