Three Big Books

Tuesday, August 26, 2014

Evidence of human herpesvirus-6 and -7 reactivation in miscarrying women with pityriasis rosea.

Background on HHV-6:

No surprise to anyone who knows anything about CFS, AIDS or HHV-6

CDC Whistleblower: The CDC deliberately altered autism data

Konnie Knox's new HHV-6 business

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.

Some of the most interesting statements about HHV-6

"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
"As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV." --Konnie Knox
"It seems wherever HHV-6 is going, you're bound to bump into HIV. It's like a cohabitation." --Robert Gallo
"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
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 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-infectd AIDS patiens, and she now wanted to know how HHV-6 was capable of knocking out those cells. Her tests showed that, besides destroying macrophages, HHV-6 interfered with the normal functioning of the scavenger cells by blocking the release of a type of oxidant, a substance the cells normally generate to attack microbes. Knox noted that HIV was not known to be capable of this specific type of action. She concluded that, at the very least, HHV-6 could contribute to the depletion of the macrophages in the lungs. This in turn woud weaken the immune system, leaving the body vulnerable to a host of infections that were normally well controlled. Did HHV-6 help HIV destroy macrophages in the lungs? Not necessarily. HHV-6 apparently had the potential to do a brutally effective job on its own. Perhaps HIV was giving HHV-6 a boost, not the other way around. Or more provocative yet, Knox wondered, was HIV doing any killing in the body, or was HHV-6 the lone assassin? Clearly, heresy was incubating in the Milwaukee wing of AIDS science. --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

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