Friday, November 20, 2015

Let's get it straight.

December 1 isn't World AIDS Day.

It's World Chronic Fatigue Syndrome 
Cover-up Day


Please send an email to Dr. Francis Collins, the Director of the National Institutes of Health.



Francis S. Collins
Director of the National Institutes of Health 
9000 Rockville Pike
Bethesda, Maryland 20892

Dear Dr. Collins:

It's time that the public knew about all the diseases HHV-6 is causing in our society. The days of using the fraudulent HIV paradigm of AIDS to cover up the HHV-6 pandemic must come to an end!

You shouldn't try to control panic about HHV-6 by lying to the public.

I urge you to support the goals of International HHV-6 Protests and Teach-ins that will be taking place at universities all over the world during the next several years.
Those goals include the support of freedom of thought, speech and dissent in science in general and in research of HHV-6-related diseases in particular. HHV-6-releated diseases include so-called "AIDS" and "Chronic Fatigue Syndrome," but are by no means limited to them. I also urge you to declare your support of the Harvard Declaration of the HHV-6 Rights of Man.


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 belied 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.

Sincerely,

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

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

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

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




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

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

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

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

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

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

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

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

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

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

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

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

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

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


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