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Sunday, June 22, 2014

A case of bilateral human herpes virus 6 panuveitis with genomic viral DNA integration

http://www.joii-journal.com/content/4/1/16/abstract

Conclusions

HHV-6 should be considered in the differential for infectious uveitis in immunocompromised hosts who may otherwise have a negative work-up. HHV-6 DNA integration may lead to difficulties in disease diagnosis and determining disease resolution.

Wednesday, June 11, 2014

One of the most important papers ever published on HHV-6

http://www.journalofclinicalvirology.com/article/S1386-6532%2809%2900194-2/abstract

Conclusion

These results imply that HHV-6A, either in latent form or during acute infection, directly transactivates HERV-K18. This HERV-K18 induction may be mediated through IFN-α that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.



Wikipedia on Superantigen:


Superantigens (SAgs) are a class of antigens which cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs can be produced by pathogenic microbes (including viruses, mycoplasma, and bacteria)[1] as a defense mechanism against the immune system.[2] Compared to a normal antigen-induced T-cell response where .0001-.001% of the body’s T-cells are activated, these SAgs are capable of activating up to 25% of the body’s T-cells.[citation needed] Furthermore, Anti-CD3 and Anti-CD28 Antibodies (CD28-SuperMAB) have also shown to be highly potent superantigens (and can activate up to 100% of T cells).
The large number of activated T-cells generates a massive immune response which is not specific to any particular epitope on the SAg thus undermining one of the fundamental strengths of the adaptive immune system, that is, its ability to target antigens with high specificity. More importantly, the large number of activated T-cells secrete large amounts of cytokines, the most important of which is Interferon gamma. This excess amount of IFN-gamma in turn activates the macrophages. The activated macrophages, in turn, over-produce proinflammatory cytokines such as IL-1, IL-6 and TNF-alpha. TNF-alpha is particularly important as a part of the body's inflammatory response. In normal circumstances it is released locally in low levels and helps the immune system defeat pathogens. However when it is systemically released in the blood and in high levels (due to mass T-cell activation resulting from the SAg binding), it can cause severe and life-threatening symptoms, including shock and multiple organ failure.

All this raises the question: Are AIDS and CFS (for starters) HHV-6-mediated superantigen diseases?

HHV-6 and Sepsis

http://medicalxpress.com/news/2014-06-dormant-viruses-re-emerge-patients-lingering.html

CFS Documentary Filmmaker Ryan Pryor on Stanford MedicineX

Infection rates increasing for CFS, ME

http://www.newstalkzb.co.nz/auckland/news/nbhea/1026551465-infection-rates-increasing-for-cfs--me

Saturday, June 07, 2014

A growing body of research shows HHV-6 is the Sine Qua Non of CFS and AIDS.





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 http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html
"As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV." --Konnie Knox http://www.chronicillnet.org/online/Knox.html
"It seems wherever HHV-6 is going, you're bound to bump into HIV. It's like a cohabitation." --Robert Gallo http://www.aegis.com/news/newsday/1992/ND920206.html
"All the evidence now available indicates that of the two viruses, HIV and HHV-6A, the most destructive by far is HHV-6A which has all the characteristics of African Swine Fever virus." --Mark Konlee
"The evidence that CFS may reflect human infection with mouse retroviruses (XMRV and the polytropic murine leukemia viruses (MLVs) has been seriously challenged. However this does not alter the evidence of neurological dysfunction in CFS, and it does not have a bearing on evidence linking CFS with other neurotropic viruses--particularly human herpesvirus six and enteroviruses." --Anthony Komaroff, Nature Reviews Neuroscience, advance online publication, Published online 27 July 2011
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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