Bulletin #65 from the Coordinating Committee of The International HHV-6 Protest and Teach-in At Harvard (November 9-11, 2015)
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.
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
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
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
The Larry Kramer of HHV-6 activism has been found!
Please post this on all social media
and help the message go viral!
The International HHV-6 Protest
Thousands of civil rights activists and public health activists should meet at Harvard during the HHV-6 Foundation's International Conference on HHV-6 & 7 (November 9-11, 2015) to start a new HHV-6 public health and civil rights movement.
They should demand reparations for everyone who has been harmed by the HIV Fraud Ponzi Scheme and the HHV-6 Cover-up.
They should also demand that key players in the HIV Fraud Ponzi Scheme and HHV-6 Cover-up be removed from positions of power and science and medicine: Robert Gallo, Luc Montagnier, Anthony Fauci, Dharam Ablashi, Anthony Komaroff, Henri Agut, Dharam Ablashi, Myron Essex and Phil Pellet.
Harvard should consider cancelling classes for three days for a HHV-6 Teach-in. HHV-6 will affect the future of every student at Harvard as well as every person on this planet. It deserves this kind of attention.
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 20Although 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 69The 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
The Larry Kramer of HHV-6 activism has been found!
Please post this on all social media
and help the message go viral!
The International HHV-6 Protest
and Teach-in At Harvard
During the HHV-6 Foundation's 9th International
Conference on HHV-6 & 7
During the HHV-6 Foundation's 9th International
Conference on HHV-6 & 7
November 9-11, 2015
First protest outside the cocktail reception Sunday, November 8th from 5:00pm – 7:00pm
First protest outside the cocktail reception Sunday, November 8th from 5:00pm – 7:00pm
Overview
Thousands of civil rights activists and public health activists should meet at Harvard during the HHV-6 Foundation's International Conference on HHV-6 & 7 (November 9-11, 2015) to start a new HHV-6 public health and civil rights movement.
They should demand reparations for everyone who has been harmed by the HIV Fraud Ponzi Scheme and the HHV-6 Cover-up.
They should also demand that key players in the HIV Fraud Ponzi Scheme and HHV-6 Cover-up be removed from positions of power and science and medicine: Robert Gallo, Luc Montagnier, Anthony Fauci, Dharam Ablashi, Anthony Komaroff, Henri Agut, Dharam Ablashi, Myron Essex and Phil Pellet.
Harvard should consider cancelling classes for three days for a HHV-6 Teach-in. HHV-6 will affect the future of every student at Harvard as well as every person on this planet. It deserves this kind of attention.
(More to come.)
Visit the International HHV-6 Protest
and Teach-in at Harvard Website.
THE CONFERENCE'S ORGANIZING COMMITTEE, SESSION CHAIRS & INVITED SPEAKERS (LIST IN FORMATION)
More on the HHV-6 Conference here.
Please sign the Harvard Declaration of the HHV-6 Rights of Man and send it today to Francis S. Collins, the Director of the National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892
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
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.
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.)
Black Lives Matter.
Gay Lives Matter.
The Truth about
HHV-6 Matters.
Books participants in the International HHV-6 Protest and Teach-in at Harvard (November 9-11, 2015) should read
in preparation for the big event:
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)
SCIENCE SOLD OUT: DOES HIV REALLY CAUSE AIDS?
The Closing Argument by Charles Ortleb (Available on Kindle and in a Print Edition. Free for Kindle owners with Amazon Prime.)
Visit the International HHV-6 Protest
and Teach-in at Harvard Website.
THE CONFERENCE'S ORGANIZING COMMITTEE, SESSION CHAIRS & INVITED SPEAKERS (LIST IN FORMATION)
Philip E. Pellett, PhD, Wayne State University, Co-Chair
Louis Flamand, PhD, MBA, Laval University, Co-Chair
Anthony L. Komaroff, MD, Harvard Medical School, CME Chair & Host
Dharam Ablashi, DVM, HHV-6 Foundation
Henri Agut, MD, PhD, Groupe Hospitalier Pitié-Salpêtrière
Michael Boeckh, MD, PhD, Fred Hutchinson Cancer Research Center
Mary T. Caserta, MD, University of Rochester Medical Center
Vincent Descamps, MD, Bichat Claude Bernard Hospital
Dario DiLuca, PhD, University of Ferrara
Leon G. Epstein, MD, Northwestern University, Feinberg School of Medicine
Niza Frenkel, PhD, Tel Aviv University
Agnes Gautheret-Dejean, MD, PhD, Groupe Hospitalier Pitie-Salpetriere
Ursula Gompels, MSc, PhD, London School of Hygiene and Tropical Medicine
Per Höllsberg, MD, Aarhus University
S. David Hudnall, MD, Yale University School of Medicine
Amy Hudson, PhD, Medical College of Wisconsin
Steven Jacobson, PhD, National Institute of Neurological Disorders and Stroke
Ruth Jarrett, MD, University of Glasgow
Benedikt Kaufer, PhD, Free University of Berlin
Irmeli Lautenschlager, MD, PhD, Helsinki University Hospital and University of Helsinki
Ann Leen, PhD, Baylor College of Medicine
Per Ljungman, MD, PhD, Karolinska University Hospital
Paolo Lusso, MD, PhD , National Institute of Allergy and Infectious Diseases
G. Peter Medveczky, MD, University of South Florida
Yasuko Mori, MD, PhD, Kobe University Graduate School of Medicine
Lieve Naesens, PhD , Rega Institute, Katholieke Universiteit Leuven
Raymund R. Razonable, MD, College of Medicine, Mayo Clinic
Nicola Royle, PhD, University of Leicester
Lawrence J. Stern, PhD, University of Massachusetts Medical School
Koichi Yamanishi, MD, PhD, Osaka University
Tetsushi Yoshikawa, MD, Fujita Health University School of Medicine
Katherine N. Ward, MD, University College London
Danielle Zerr, MD, University of Washington & Seattle Children’s Hospital
Sponsored by: HHV-6 Foundation, Dharam Ablashi, Scientific Director
Louis Flamand, PhD, MBA, Laval University, Co-Chair
Anthony L. Komaroff, MD, Harvard Medical School, CME Chair & Host
Dharam Ablashi, DVM, HHV-6 Foundation
Henri Agut, MD, PhD, Groupe Hospitalier Pitié-Salpêtrière
Michael Boeckh, MD, PhD, Fred Hutchinson Cancer Research Center
Mary T. Caserta, MD, University of Rochester Medical Center
Vincent Descamps, MD, Bichat Claude Bernard Hospital
Dario DiLuca, PhD, University of Ferrara
Leon G. Epstein, MD, Northwestern University, Feinberg School of Medicine
Niza Frenkel, PhD, Tel Aviv University
Agnes Gautheret-Dejean, MD, PhD, Groupe Hospitalier Pitie-Salpetriere
Ursula Gompels, MSc, PhD, London School of Hygiene and Tropical Medicine
Per Höllsberg, MD, Aarhus University
S. David Hudnall, MD, Yale University School of Medicine
Amy Hudson, PhD, Medical College of Wisconsin
Steven Jacobson, PhD, National Institute of Neurological Disorders and Stroke
Ruth Jarrett, MD, University of Glasgow
Benedikt Kaufer, PhD, Free University of Berlin
Irmeli Lautenschlager, MD, PhD, Helsinki University Hospital and University of Helsinki
Ann Leen, PhD, Baylor College of Medicine
Per Ljungman, MD, PhD, Karolinska University Hospital
Paolo Lusso, MD, PhD , National Institute of Allergy and Infectious Diseases
G. Peter Medveczky, MD, University of South Florida
Yasuko Mori, MD, PhD, Kobe University Graduate School of Medicine
Lieve Naesens, PhD , Rega Institute, Katholieke Universiteit Leuven
Raymund R. Razonable, MD, College of Medicine, Mayo Clinic
Nicola Royle, PhD, University of Leicester
Lawrence J. Stern, PhD, University of Massachusetts Medical School
Koichi Yamanishi, MD, PhD, Osaka University
Tetsushi Yoshikawa, MD, Fujita Health University School of Medicine
Katherine N. Ward, MD, University College London
Danielle Zerr, MD, University of Washington & Seattle Children’s Hospital
Sponsored by: HHV-6 Foundation, Dharam Ablashi, Scientific Director
More on the HHV-6 Conference here.
Please sign the Harvard Declaration of the HHV-6 Rights of Man and send it today to Francis S. Collins, the Director of the National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892
The Harvard Declaration of the HHV-6 Rights of Man
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.
36. The right not to be lied to about the the impact of HHV-6 on Dendritic Cells.
37. The right not to be lied to about the the impact of HHV-6 infection of the brain.
38. The right not to be lied to about the the impact of HHV-6 infection of the liver.
39. The right not to lied to about the ability of HHV-6 to affect cytokine production.
40. The right not to be lied to about the ability of HHV-6 to affect Aortic and Heart Microvascular Endothelial cells.
41.
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.
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)
The name of Chronic Fatigue Syndrome should be changed to AIDS Spectrum Virus Syndrome
(AIDS Virus Syndrome or ASVS.)
Black Lives Matter.
Gay Lives Matter.
The Truth about
HHV-6 Matters.
Books participants in the International HHV-6 Protest and Teach-in at Harvard (November 9-11, 2015) should read
in preparation for the big event:
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)
SCIENCE SOLD OUT: DOES HIV REALLY CAUSE AIDS?
The Closing Argument by Charles Ortleb (Available on Kindle and in a Print Edition. Free for Kindle owners with Amazon Prime.)
The HHV-6 Cover-up Must End!
