Welcome to the site that explores the many disturbing truths about HHV-6
Is HHV-6 the viral trigger for Chronic Fatigue Syndrome, Autism and AIDS? Is it time to abandon the failed HIV paradigm of AIDS for an HHV-6 paradigm of AIDS?
Ubiquitous and very harmful, HHV-6 is the ultimate stealth virus and perhaps the greatest masquerader of all pathogens
If the stealth virus, HHV-6, is a universal infection, then it is a universal medical catastrophe. HHV-6 is such a unique virus capable of causing so many different pathologies (including HERV-K18) that it should be put in a class by itself and called a "metavirus." A "metavirus" would be one that 1) infects more than one species, 2) is spread in multiple ways 3) is capable of multiple manifestations ranging from acute and terminal to chronic and inapparent, and 4) is capable of infecting every organ in the body and causing a wide variety of pathologies and symptoms. 5)Is capable of becoming chromosomally integrated 6) Is so versatile and widespread that it makes it difficult to distinguish epidemiologically between cases and controls.
Chromosomally Integrated HHV-6 (CIHHV-6) May Be the new face of the HHV-6 Spectrum Pandemic
Because HHV-6 has been ignored for a quarter of a century while scientists stubbornly focused on the wrong virus in AIDS, there is now an epidemic of chromosomally integrated HHV-6 (CIHHV-6) to contend with. People with CIHHV-6 may have very serious immunodeficiency problems and be at increased risk for a number of cancers.
A very special welcome to visitors to the HHV-6 Site from Russia.
Thank you for visiting. The explosive epidemic of African Swine Fever in your country should be watched closely. We urge you to press scientists and doctors in your country to look closely at the possibility that African Swine Fever Virus can infect people and when it does, will be mistaken for HHV-6 or HHV-7 or HHV-8. See this page for more information.
Breaking News!
Anti-malarial drug may prove useful for the treatment of HHV-6
Sensitivity of human herpesvirus 6 and other human herpesviruses to the broad-spectrum antiinfective drug artesunate
"Artesunate possesses anti-HHV-6 activity in vitro and may be useful for treatment of HHV-6 infections." --Jens Milbradt, Sabrina Auerochs, Klaus Korn, Manfred Marschall Journal of Clinical Virology, Volume 46, Issue 1, Pages 24-28 (September 2009)
The Cost of HHV-6 Denialism: Untreated HHV-6 May Be Causing Brain Cancer in Children.
Detection of human herpesvirus-6 variants in pediatric brain tumors: association of viral antigen in low grade gliomas.
BACKGROUND: Human herpesvirus-6 (HHV-6) has been associated with a diverse spectrum of central nervous system (CNS) diseases and reported glial tropism. OBJECTIVE: To determine if HHV-6 is present in a series of pediatric brain tumors. STUDY DESIGN: Pediatric gliomas from 88 untreated patients represented in a tissue microarray (TMA) were screened for HHV-6 by nested polymerase chain reaction (PCR), in situ hybridization (ISH), and immunohistochemistry (IHC) and compared to non-glial tumors (N=22) and control brain (N=32). Results were correlated with tumor grade and overall survival. RESULTS: HHV-6 U57 was detected by nested PCR in 68/120 (57%) tumors and 7/32 (22%) age-matched non-tumor brain (P=0.001). HHV-6 U31 was positive in 73/120 (61%) tumors and 11/32 (34%) controls (P=0.019). Seventy-two percent (43/60) of tumors were HHV-6 Variant A. HHV-6 U57 was confirmed by ISH in 83/150 (54%) tumors and 10/32 (31%) controls (P=0.021), revealing a non-lymphocytic origin of HHV-6. HHV-6A/B gp116/64/54 late antigen was detected by IHC in 50/124 (40%) tumors and 6/32 (18%) controls (P=0.013). Interestingly, 58% of low grade gliomas (N=67) were IHC positive compared to 19% of high grade gliomas (N=21, P=0.002) and 25% of non-gliomas (N=36, P=0.001). HHV-6A/B gp116/64/54 antigen co-localized with glial fibrillary acidic protein, confirming the astrocytic origin of antigen. Overall, there was no primary association between HHV-6A/B gp116/64/54 antigen detection and survival (P=0.861). CONCLUSIONS: We provide the first reported series of HHV-6 detection in pediatric brain tumors. The predominance of HHV-6 in glial tumors warrants further investigation into potential neurooncologic disease mechanisms.
--Crawford JR, Santi MR, Thorarinsdottir HK, Cornelison R, Rushing EJ, Zhang H, Yao K, Jacobson S, Macdonald TJ. J Clin Virol. 2009 Sep;46(1):37-42. Epub 2009 Jun 7
"The exploration of HHV-6 and AIDS has been an interesting journey for me. Ten years ago a colleague of mine, a fellow M.D., told me he was absolutely convinced that HIV did not cause AIDS. I thought he was a bit out of touch with reality. Turns out I was wrong, and while the AIDS story has not yet been fully told, I no longer believe that HIV is the one and only cause of this worldwide epidemic."--Dennis Gersten, M.D. The HHV-6 Viral Menace
Human herpesvirus 6 (HHV-6) infected cells were detected in all lung, lymph-node, spleen, liver, and kidney tissues obtained at necropsy from an unselected series of nine patients with AIDS. This infection rate was significantly higher than that for cytomegalovirus. Lung infection with HHV-6 was extensive enough in one patient to account for fatal pneumonitis. In other tissues increased numbers of HHV-6 infected cells were related to the presence of lymphocytes infiltrates or residual lymphoid tissue, with lymphocytes being predominantly infected. Thus HHV-6 is an important pathogen in patients with AIDS.--Knox KK, Carrigan DR., Department of Pathology, Medical College of Wisconsin, Milwaukee 53226. Lancet. 1994 Mar 5;343(8897):577-8.
"With the SIV alone, there was a little immune deficiency, and with the HHV-6 alone nothing, but with the two together they got it. I think we have proven the point with that rhesus virus and that we can publish that soon. So, I believe human herpesvirus-6 is a factor in AIDS progression. " --Robert Gallo in 1995 http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html
The HHV-6 Site is devoted to ending HHV-6 denialism and raising awareness about an insidious virus that may be the cause of a variety of diseases that include AIDS, CFIDS, M.S, Autism, COPD, ADHD, and assorted cancers, neurological disorders, respiratory syndromes and cardiac problems.
The politics of HHV-6 are essentially the politics of HIV and AIDS. If HHV-6 had been discovered before HIV it would have probably been declared the real cause of AIDS. Unfortunately, by 1986 when HHV-6 was discovered, an AIDS establishment had carved the definition and cause of AIDS in stone.
The victims of the politics of HIV and HHV-6 are not just AIDS patients. HHV-6 is a dynamic virus that may be behind a great many of so-called mysterious diseases today--all of which will be explored on this site.
The real mystery is that reasonable men and women do not see what HHV-6 is and what it is causing. It's not rocket science.
The Real Thing:
Dr. Konstance Knox explains why HHV-6 may be the key to dealing with AIDS.
by Neenyah Ostrom
New York Native, issue #678, April 15, 1996
Konstance Knox, Ph.D., is an HHV-6 researcher who has just published a study with extraordinary implications for AIDS research and treatment strategies. Along with colleague Donald R. Carrigan, Ph.D., Knox demonstrated that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6 Variant A infections in their lymph nodes early in the course of their disease. Seventy-five percent of these patients, in fact, had CD4 cell counts higher than 200 (the cut-off for receiving a diagnosis of AIDS), up to as high a CD4 count as 700. This finding led Knox and Carrigan to conclude that "active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that the A variant of HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS." This new study, in other words, presents data further implicating HHV-6, particularly Variant A (HHV-6A), as a cofactor (at the very least) in the development of AIDS. (The report is "Active HHV-6 Infection in the Lymph Nodes of HIV Infected Patients: In Vitro Evidence That HHV-6 Can Break HIV Latency," published in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology," April 1, 1996.) Knox, who has a Ph.D. in Experimental Pathology from the Medical College of Wisconsin, is currently conducting cancer research in the Immunotherapy Program at St. Luke's Medical Center in Milwaukee, Wisconsin. She spoke to the Native on the day following publication of the new study.
Neenyah Ostrom: What is the bottom line, with respect to your new findings? Is it that Human Herpes Virus 6 (HHV-6) is present from the beginning of what we define as AIDS?
Dr. Konstance Knox: HHV-6 is present from very early in HIV infection. So we're not talking about waiting until people have opportunistic infections, and CD4 counts between 100 and 200. We're finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB. The only opportunistic infections that you see in AIDS patients with CD4 counts above even 100 are TB and Herpes simplex and Herpes zoster. And all three of those, of course, also infect healthy people and cause disease. So, what we found, when we examined the lymph node biopsies of HIV-infected patients, was HHV-6. We found both variants of HHV-6-HHV-6A and HHV-6B-but the predominant virus was HHV-6A. And we're talking about finding the virus in lymph nodes of patients with CD4 counts of over 700. The mean CD4 count of 75 percent of the patients we examined was approximately 300. (There was a total of ten patients in this study just published, and we had CD4 counts on eight of them.) That's a unique finding. And one of the patients had a CD4 count of 711. So why is that virus, HHV-6A, there? My personal impression, because of where we find HHV-6A-we find a predominance of infection in the germinal center of the lymph node, which is where we know HIV hangs out-is that the tat protein of HIV stimulates HHV-6A replication. And in the study that we have just published, the one that came out yesterday [April 1], we showed that HHV-6A causes an increase in HIV production. These findings are not based solely on this one study. We have done subsequent studies, and there is another already-published study by Charles Wood from Miami also demonstrating that tat protein from HIV induced more HHV-6A production. So the theory-what seems reasonable to us-is, because these viruses hang out in the same place, and they infect the same cells, that it's not an accident that they co-localize-where you find HIV, you find HHV-6A. I think that there is a mutual enhancement and potentially almost a mutual dependency for efficient replication. My impression is that HIV kind of acts as a wet nurse to HHV-6A, because in all the other immunocompromised patients that we have looked at-and primarily, these are bone marrow transplant patients-we don't find the A variant of the virus. We don't find it, and the best guestimates of how many people are infected with type A-well, the numbers are sketchy. Because of the blood tests previously available, we only know about type B. You know, the classic numbers are that 90 percent of people by the age of two are infected with HHV-6. But that's the B variant, not the A variant. And the best estimate, up to about the age of 12, is that about five to 15 percent of people are infected with variant A. The epidemiology of HHV-6A infection has not been done. Now, it's kind of curious to me why the studies have not been done. You know, there's been a lot of sort of pooh-poohing about the role of HHV-6 in AIDS. I think that's because people look at it, and they say, well, everybody's infected with HHV-6 by the age of two. Yes, everybody's infected with the B variant. But we don't know how many people are infected with the A variant. We've just completed a study that we have submitted in which we examined 22 HIV-positive and AIDS patients. Every one of them has active replication of HHV-6A and it doesn't matter what stage of disease they're in, from frank AIDS, to autopsies, all the way up to people with CD4 cell counts of over 700. We believe there is a special interaction between HIV and HHV-6A.
N. Ostrom: How different are variants B and A from each other?
K. Knox: Do you mean biologically?
N. Ostrom: Yes. I've heard speculation that they should have been classified as two different viruses, or that, conversely, HHV-7 is no more different from the two HHV-6 variants than they are from each other.
K. Knox: HHV-7 is probably more akin to HHV-6B. There was an interesting study-and it was a PCR [polymerase chain reaction, i.e. "DNA amplification"] study-which basically showed that, if you were to analyze peripheral lymphocytes, you can find HHV-7 and HHV-6B in about 83 percent and 25 percent of healthy people, respectively. HHV-6A is found much, much less frequently. We're talking about a very small percent-five percent of people. HHV-6A is different. Probably a general rule of thumb is that HHV-6A can do everything that B can do, and more. And it's also much more destructive. It is a very destructive virus. It's more similar to what people think of when they think of a herpes virus. It is very lytic-it kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow. In all the dozens to hundreds of transplant patients we've looked at, if we find HHV-6 disease, it's variant B. We have only seen HHV-6A in, I think, five different individuals, from whom we've isolated it or stained it in tissues. These are not HIV-positive individuals. So, we found HHV-6A in five out of 100 or so patients. Four of those patients were dead. It is very destructive.
N. Ostrom: The question then becomes, in my mind, can HHV-6A do everything that HIV can do?
K. Knox: As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV. And these are data from many people's laboratory studies, and that includes Paolo Lusso and Robert Gallo, as well as our own. Where we have seen HHV-6A in tissue, we see dead tissue. And where you see HIV-you know, you can have HIV alone, and you may see some reactive changes, like the immune system reacting to a viral infection as if you have flu or something like that. But you don't see dead tissue. You don't see destroyed organs and scar formation, and that's what you see when you see HHV-6A. We find replacement of the normal architecture of the lymph nodes with scar tissue. HHV-6A kills it. It kills the lymph node tissue. If I were to place my bets-I do think the viruses HIV and HHV-6A are interactive. I think one of the reasons why you almost always find both of them is that there are viral products, some of the gene products that they make, that enhance each other's replication. I think they're a team. And, when the two of them are present, they induce the production of more of each other. It's a mutually enhancing relationship. It's our feeling that if you could interrupt or limit or suppress the HHV-6A infection, the levels of HIV would go down tremendously and HIV would become just a chronic viral infection. And, potentially, the antiviral agents that are out there would be able to manage that. We don't have any evidence, looking in the tissue, that HIV is responsible for any of the destruction. And, if you think about it, HIV infects patients for years-a decade or more-without progressing to AIDS. When you look in their tissues, you have to ask how you can have such a long-term viral infection and have no damage? Then something seems to happen somewhere in their course of disease. In some people, it happens earlier; in some people, it happens later; and there's that small percentage of people in whom it never seems to happen at all. Our hypothesis would be that, if we were to look in the lymph nodes of the long-term non-progressors, we would not find HHV-6A.
N. Ostrom: Do you have plans to do that study?
K. Knox: Well, last December I contacted Giuseppe Pantaleo-he's with Tony Fauci's group [at the National Institutes of Health], who had published the New England Journal of Medicine paper just about a year ago on the progressors and long-term non-progressors and the difference in the lymphoid organs between the two. The basic difference is, in the non-progressors, even though they have replication-competent HIV, they don't have any evidence of degeneration or destruction of their tissue, even though HIV is there. So the hypothesis would be that those few percentage of HIV-infected patients that are long-term non-progressors don't have HHV-6A replicating in their lymph node tissues. Pantaleo has agreed to send us what the NIH has in the way of tissues from that study. Now, I've been waiting-you know, they had the furlough, and all this other kind of stuff. And then I met with Dr. Pantaleo, actually, about the middle of February, and he again reiterated that he would be sending those tissues to me. Thus, he has personally assured me, but, until I have the tissues, we can't do the direct test of the hypothesis.
N. Ostrom: Why can't we get more funding for this research?
K. Knox: Well, I don't know if you've been tracking the kinds of exposes that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there's been a real resistance to entertaining hypotheses or directions of AIDS research that aren't looking specifically at HIV, and that is the basic problem. Our studies themselves have been enthusiastically received, but the funding hasn't followed. And that is funding through the federal agencies-like the NIH-and I think one of the things that has stopped that has been the confusion with HHV-6B. People think, well, if everybody's infected with HHV-6, why doesn't everybody have AIDS? Well, we're all infected with HHV-6B, but there's probably only a very small percentage of people infected with HHV-6A. And there's a very unique relationship between A and HIV-when we examine HHV-6B and HIV together, we don't see the same effects. They don't have the same interaction. So, we're talking about two different viruses, essentially, A and B. And people have merged the two into just HHV-6 and have not appreciated the biologic differences between the two viruses. And actually, in our own research, this has only been clarified in the last year. In our earlier studies, we only had reagents to look at HHV-6. We did not have the specific reagents to separate the two when we looked in the tissue; we could not tell if it was A or B. It's only been in the past year that we have developed the technologies to be able to distinguish between the two.
N. Ostrom: So you now have very reliable testing that will distinguish between Variant A and Variant B?
K. Knox: Yes.
N. Ostrom: Is it antibody testing, or DNA testing?
K. Knox: It is antibody testing. You could do both, but we use antibody testing.
N. Ostrom: And you test blood? Or do you look only at tissues?
K. Knox: We do tissue biopsies. We look in the tissue itself. And it is very difficult for people to dismiss the idea of HHV6-A because, frankly, nobody knows what the epidemiology is, how many healthy people are infected, how it's transmitted, those kinds of things. We don't know. And there is a unique kind of collaboration between HHV-6A and HIV that HHV-6B does not have. HHV-6B does cause disease. It kills immunocompromised patients. It kills transplant patients. But, with respect to AIDS and HIV infection, we believe that the A variant is what is important, because it has this special interaction with HIV. And variant A is in all the AIDS patients. You don't find it, even in other immunocompromised patients, like bone marrow transplant patients. There is something special about the interaction of the two viruses, HIV and HHV-6A.
N. Ostrom: Do you think they might have evolved together?
K. Knox: Actually, that is a very interesting thing to think about. Yes, I think that they have evolved together, and I think they really like hanging out together. There seems to be a selective advantage to the two viruses being in close proximity-and the tat protein of HIV is something HHV-6A seems to like. There's something that HHV-6A makes as well that, in our laboratories, gets HIV really revved up. If there's an advantage, viruses evolve together. If selective pressures are put on them, they will respond to make their environment more compatible. Viruses want to make more of themselves. They don't destroy things on purpose, because it's actually not to their advantage. It wouldn't surprise me, in their natural histories, if HHV-6A and HIV evolved together, because there's such an enhancement of the two viruses when they're together. Although in vitro (laboratory) studies published over the last eight or ten years have suggested a synergy between HIV and HHV-6A, in vivo (in the body) evidence has been lacking. Finally, we have examined the tissue of HIV-infected patients and asked, why do all these people have HHV-6A replicating in their tissues when they're still healthy, and we can't even find it in other immunocompromised patients? It's a very provocative finding. There's also a study you'll find interesting, that was performed by Italian researcher Dario Diluca, published in the Journal of Clinical Microbiology, I think. Dario has also been doing HHV-6A and HIV research. What he just published last summer is a PCR study of HHV-6 in Chronic Fatigue Syndrome patients. The unique finding concerned HHV-6A. Whereas you can find it in the peripheral lymphocytes of about four percent of healthy people, you see it in 22 percent of Chronic Fatigue Syndrome patients. There's no difference in the levels of HHV-7 and HHV-6B in healthy people and CFS patients, but the A variant was seen at four percent in healthy people and 22 percent in CFS patients, which is very significant.
N. Ostrom: In their natural killer cell paper, Lusso and Gallo showed that HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. They identified the problem in both sets of patients, so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.
K. Knox: Yes, it's a very disregulating virus. Variant B is not benign, but variant A is especially destructive. This is not only when we look at tissues, but also in the test tube-variant A is especially destructive. Which antiviral drugs do you know have effectiveness against HHV6-A? We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. Actually, with foscarnet, we have treated specifically HHV-6A infections and seen very nice reversals of clinical syndromes. We don't always know which variant we're treating when we're treating HHV-6. Also, if you look in the literature, there are three major studies looking at acyclovir in AIDS patients. These were patients with CD4s of less than 150. There was one study in particular that I'm recollecting in which there were about 300 patients. They treated half with AZT alone, and half with AZT plus acyclovir. What they wanted to do was to look to see if acyclovir could suppress CMV reactivation. Well, what they found was that it had no effect on CMV infection, but there was a curious, significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone. There are three major studies in the literature like that, and the speculation as to why that is? They don't know. And they don't address it, because they haven't got a clue as to why it might be. Now, we have never treated HHV-6 infections with acyclovir, because the B variant of the virus is resistant, and that's usually the virus that we see in transplant patients. But in laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than ganciclovir, and if you're talking about treating healthy people in a clinical trial, you're looking for something that people can take orally. You don't want them to have to come in for IV infusions, and foscarnet would require that. So I would say that acyclovir and its analogs and ganciclovir would be very interesting.
N. Ostrom: So, what you have discovered should be viewed as good news?
K. Knox: Oh, I think it's tremendously good news. I think it offers the best hope that we've seen in 15 years of this epidemic. That's because it's the first new approach. And the difference is that we believe that actually what destroys the immune organs, the lymph nodes, is HHV-6A. It is not HIV. HIV keeps it going, and HHV-6A keeps goosing HIV, and together they keep secreting products that each other love. They stroke each other. And that's a hard team to break up. You can't do it just by targeting HIV.
N. Ostrom: Is there anything else you'd like people to know about your research?
K Knox: Now that we've made the distinction between the two HHV-6 viruses, A and B, we're really hoping that funding is loosened up and the abuses of how AIDS research has been managed by the government agencies, by NIH-certainly, we've been caught in that trap. I just hope that they loosen up soon enough that we don't have to abort our program. And it's getting pretty close. It's pretty close. http://www.chronicillnet.org/online/Knox.html
Help Raise Awareness about the HHV-6 Spectrum Pandemic.
Purchase these books and share them with your friends and family.
The Closing Argument
By Charles Ortleb
The world's first work of fiction based on the cover-up of the HHV-6 Spectrum Pandemic and its impact on the African-American community.If you read only one book about AIDS in your entire life, it should be this one. I does for AIDS what "Uncle Tom's Cabin" did for slavery. A print version of this book and a Kindle version are also available at Amazon.com. This controversial novella uses a criminal trial to tell the story of an African-American man accused of spreading AIDS in New England. His lawyer takes the bold step of turning the tables on the government and the AIDS medical establishment. He tries to convince the jury that due to racism and homophobia, the wrong virus has been blamed for AIDS. He brings scientists into the courtroom to present information about AIDS that most of the public is unaware of, data about HIV and a virus called HHV-6 which raise serious doubts that HIV is the real culprit in AIDS. The defense attorney is mysteriously killed hours after presenting his closing argument and there is no verdict delivered in the book . The reader is put in the jury box and has to decide if most of what we have been told about AIDS is false. Do you believe everything you've been told by the AIDS establishment? You won't after you read "The Closing Argument." Nicholas Regush, the late ABC News Producer for Peter Jennings said the book was "Eye-popping reading if you dare to expand your scope of thinking about AIDS and justice." In addition to presenting a pioneering and dramatic analysis of the racist and heterosexist politics of the AIDS epidemic, this is the first work of fiction to talk about HHV-6, the virus that is increasingly being recognized as the real problem in AIDS rather than HIV, and also as the probable cause of many other so-called mysterious epidemics of immune dysfunction like Chronic Fatigue Syndrome.
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
A primer on HHV-6, AIDS and Chronic Fatigue Syndrome by the one of the most important CFS and AIDS journalists in the world.
The Virus Within: A Coming Epidemic
By Nicholas Regush
Amazon.com Review:
"If you were told there was a killer in your basement, you'd be legitimately concerned. Scientists have uncovered a virus living peacefully inside us that may strike out at us when our guard is down, but nobody seems to be listening. Potentially linked to such poorly understood diseases as multiple sclerosis, chronic fatigue syndrome, and AIDS, this member of the herpes family (HHV-6) is thoroughly examined in science journalist Nicholas Regush's The Virus Within. Unfortunately, little is known at present, in part because of the personality-driven nature of research funding; struggling scientists must compete with big names like Robert Gallo for attention and dollars. Regush follows the careers of Donald Carrigan and Konnie Knox, medical virologists trying to learn more about HHV-6 while at the same time informing their unconcerned colleagues about its threat.
While the book is a bit too easy on the Peter Duesberg-led charge against the HIV hypothesis of AIDS, it makes the point well that the scientific community, spurred on by clueless funders, is too quick to crystallize around one way of thinking about disease. This may be more a important issue than the threat of HHV-6--even if we do expand our research focus to include this likely killer, we haven't reached the root of the problem. How long will it take these voices in the wilderness to find sympathetic ears, and how long will it take the next scientific prophets to make themselves heard? Perhaps, if enough of us read The Virus Within, we can heed their warnings while there's still time to act." --Rob Lightner
What Really Killed Gilda Radner?: Frontline Reports on the Chronic Fatigue Syndrome Epidemic
By Neenyah Ostrom
The pioneering reporting on the relationshp between AIDS and Chronic Fatigue Syndrome by one of he world leading CFS investigative reporters.
50 Things You Should Know About the Chronic Fatigue Syndrome Epidemic
By Neenyah Ostrom
Neenyah Ostrom, author of "What Really Killed Gilda Radner? Frontline Reports on the Chronic Fatigue Syndrome Epidemic" probes all the facts and answers questions about today's most misunderstood syndrome:
- What causes it?
- Is it contagious?
- Is it a form of AIDS?
- Can it lead to cancer?
- Can children get it?
- What is the government doing about it?
- And much more
Simple. Readable. Understandable. In depth. "50 Things You Should Know About the Chronic Fatigue Syndrome Epidemic" gives you a quick but thorough look at a disease that threatens us all.
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