Three Big Books

HHV-6 and Autism

Are Autism Spectrum Disorders part of the Multisystemic HHV-6 Spectrum of Disorders?

Is the Multisystemic HHV-6 Epidemic Causing the Dramatic Rise in Autism?

Can the complications of Autism Spectrum Disorder be reduced by controlling Multisystemic HHV-6?

Why won't the Centers for Disease Control tell the truth about the role of Multisystemic HHV-6 in Autism, Chronic Fatigue Syndrome, AIDS and many other serious neuroimmunological syndromes? What exactly is Multisystemic HHV-6? Is it really just a reactivated herpes virus or is it actually some other kind of lethal virus that can be passed from person to person and can become chromsomally integrated? Does it belong in a class by itself? Where did it come from? Is it a zoonose, a virus that is circulating in people and animals?

"About six weeks back I was given the name of a woman who had approached Generation Rescue. She has a foundation which is working on the theory that the Human Herpes Virus #6 (HHV-6) is the cause of chronic fatigue syndrome. This woman’s foundation often talked with the world’s top virologists who privately tell her their belief that HHV-6 is also implicated in multiple sclerosis, autism, and seizures. She didn’t have time to pursue HHV-6 in regards to autism, but thought we should be made aware of the theory."
Kent Heckenlively, Age of Autism

Serological Association of Measles Virus and Human Herpesvirus-6 with Brain Autoantibodies in Autism

Vijendra K. Singh, Sheren X. Lin, Victor C. Yang
Clinical Immunology and Immunopathology Volume 89, Issue 1, October 1998, Pages 105-108


Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron–axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.


By Teresa Binstock
"If the autism-spectrum child's anti-HHV6 titres are elevated, you might consider evaluations of peripheral blood via PCR for HHV6 (9, 9b), which would provide an indication of the extent to which various aspects of immunity were being altered by such an infection. Interestingly, cytomegalovirus (CMV) can be present in monocytes of individuals who have no anti-CMV antibodies (9a), thus raising the possibility that HHV6 might have a similar effect in some autism- spectrum children, ie, be etiologically significant despite a lab finding of "no elevated anti-HHV6 antibodies"."


By Teresa Binstock
". . .HHV-6 (human herpes virus #6) is realized to be a common source of febrile convulsions in young children."

HIV infection in children - neurodevelopmental (autistic) outcomes and clinical pathologies - and their correlations to 'common' autism

There is a striking correlation between neurodevelopmental symptoms found in children infected with HIV virus and those children diagnosed with Autism Spectrum Disorders (of unknown aetiology). Furthermore, the underlying biomedical pathologies found in HIV-positive children are in many ways identical to biomedical pathologies found in children diagnosed with ‘common’ autism. (Editor's note: HIV-positive being a euphemism for HHV-6-positive.)

In most cases, “autism” like behaviors are caused by the break down of the child’s immune system; allowing viruses, candida, fungi and parasites to set up shop in our beautiful children’s body and brain. A better name for this condition is Neuro-Immune Dysfunction Syndrome (NIDS).
"The HHV-6 and measles viruses are etiologically linked to autism because they are related to brain autoantibodies and demyelinating diseases."
"Reports of HHV-6 and autism are abundant. Many children have high herpes titres, sometimes to that of 4-6 times of normal, often correlating with autism symptoms or seizures."
"Lauren [a child with autism] also had a huge variety of blood tests, which gave some amazing results. In basic terms it showed that Lauren’s natural killer cells were very low which shows there is a problem with her immune system, she also came up as having the HHV6 Human Herpes Virus. Lauren was over 250 times the acceptable limit. Speaking to Dr Goldberg on the phone about Lauren’s results he said it was literally one of the highest results he has seen."
"We learned, by having blood tests and immune panels prepared from our son John's blood tests (something no physician before had thought to do), that he had high HHV6 titers and low Natural Killer (NK) cells, a condition which is not caused genetically, but which is a disease probably brought on by genetic susceptibility. However, John is now curable! Treatment began a year ago, and despite two setbacks due to illness in the process, John is improving very steadily. The life described in the beginning of this short presentation has dramatically changed, in too short a period to be attributed to maturity. We have a relationship with him. We all laugh and play together now. He always listens and sometimes follows simple directions. He doesn't mess the floor anymore. He has been sleeping through the night since December. His HHV6 titers are down. Dr. Goldberg expects John to mainstream in the next two years. With your help, it could be sooner."
The symptoms of the “quiet” ADD child (who is likely connected to this phenomenon) is not consistent with the past training or processes used to “explain” and address the “hyper” ADD child. It seems likely that the cognitive defects described in adults and children with CFIDS may be thought of as milder, later-onset form of ""autism", as they are similar in symptomatology and possible etiologies. The continued exploration of an immune-dysfunctional epiphenomena, and the potential etiologies linked to it, is a door we must walk through if we expect to change the future of this generation of children!

If the Autism epidemic is being triggered by HHV-6, Ampligen may prove to be a helpful treatment that deserves a lot more research.

HHV-6 and the Promise of Ampligen

This experimental drug not only stops HHV-6, it helps AIDS and CFS patients function.

By Neenyah Ostrom
First published in: New York Native, issue #663, January 1, 1996
During 1995, a series of extremely disturbing facts were revealed about the damage Human Herpes Virus 6 (HHV-6) is able to inflict. The virus was linked to the brain and nervous system damage seen in Multiple Sclerosis; scientists warned that HHV-6 is a dangerous contaminant of the blood supply, which is not screened for its presence, and is therefore probably being transmitted via transfusion; HHV-6 was found to be the most common infection in AIDS patients, rather than CMV as was previously assumed; it was implicated as a cause of the blinding AIDS retinitis; Italian research linked HHV-6 (Variant A) not only to AIDS and Chronic Fatigue Syndrome, but also to AIDS-associated Kaposi's sarcoma; and, perhaps most importantly, HHV-6 has been shown to be present in the lymph nodes of AIDS patients right from the beginning of their disease.
All of this has resulted in a growing number of scientists who routinely refer to HHV-6 as the "AIDS co-factor."
All of this sounds pretty grim. But there is also good news to report from 1995's scientific endeavors: There is a non-toxic, experimental drug that appears to be able to stop the virus cold in its tracks. The drug is Ampligen, a special form of RNA (the sister molecule to DNA, of which most viruses are composed); it interferes with HHV-6's ability to grow.
The bad news is that the seemingly effective and non-toxic Ampligen, for some impossible-to-understand reason, has yet to be approved by the Food and Drug Administration.
In clinical trials, Ampligen not only inhibits the growth of HHV-6 in tissue culture, but also appears to produce long-term improvement in patients with CFS-who are known to have active HHV-6 infections.
Two recent studies demonstrating Ampligen's effectiveness against HHV-6, performed by some of the leading researchers in the field of the virology of HHV-6 and the clinical treatment of CFS, have added significant ammunition to arguments that Ampligen should be approved by the FDA immediately.
Dharam V. Ablashi was lead author on the scientific report, published in the journal in vivo, which showed that Ampligen inhibited HHV-6 from growing in cells in tissue culture. In addition to other collaborators, well-established CFS researchers Robert Suhadolnik and Anthony Komaroff were investigators in this study.1
Ablashi and colleagues began by pointing out that, while it is believed most people are infected with HHV-6, "many different strains of the virus, comprising of two variants (the A and B variants), with different biologic properties, have been identified." And while HHV-6 has been associated with the generally-mild childhood illness roseola, active HHV-6 infection has also been reported in a number of conditions "known or suspected to be associated with immunological dysfunction." That list, according to Ablashi and colleagues, includes AIDS, Hodgkin's disease (lymphoma), autoimmune disorders like lupus, graft-versus-host disease, and Chronic Fatigue Syndrome.2
HHV-6's possible role in AIDS is particularly troubling, Ablashi and co-workers noted, since, "Like human immunodeficiency virus-1 (HIV-1), HHV-6 is tropic for CD4-positive T-cells; dual infection of CD4-positive cells with both HIV-1 and HHV-6 greatly enhances the rate of CD4-positive cell death." They continued, "Whether the synergistic cytopathic effects of HHV-6 and HIV-1 contributes to pathology or morbidity in HIV infected patients remains to be determined." In other words, does being infected with HHV-6 in addition to HIV indicate a worse prognosis than being infected with HIV alone? The experimental drug Ampligen, Ablashi and colleagues explain, is a mis-matched, double-stranded RNA that has "broad spectrum antiviral and immune modulating activity." They note that when used in combination with "a low dose of AZT," Ampligen "significantly reduced the cytopathic effect inducted by HIV-1" in cell cultures.
As Ablashi recently told the Native, however, giving AZT to an HHV-6 infected individual can, based on laboratory findings, have an extremely deleterious effect, since AZT not only increases the growth of the virus, but increases its cell-killing ability. (See Native #662, December 25, 1995, for the complete Ablashi interview.) Ampligen has also shown a positive effect on the clinical conditions of CFS and AIDS patients, these investigators point out. In particular, a long-term trial of Ampligen treatment of CFS patients resulted in "improved performance on exercise testing as well as improved quality of life, compared to those using a placebo." Therefore, "Since HHV-6 reactivation is frequently seen in CFS infection and since Ampligen treatment seemed to produce a clinical benefit in patients with CFS, we conducted in vitro [laboratory] studies to determine whether Ampligen had antiviral effects against HHV-6."
Cells infected with the GS strain of variant A HHV-6-the type most commonly detected in patients with CFS, AIDS, and other immunocompromised conditions-were treated with Ampligen while being grown in tissue culture, before and after being infected with HHV-6. Cells that were pretreated with Ampligen before infection with HHV-6 showed "substantial inhibition of virus replication, ranging from 45.7-78.3 percent."
A second variation of the experiment was the most successful: When cells were both pre-treated with Ampligen before HHV-6 infection, and then grown in culture with Ampligen present, as well, "inhibition of virus replication was nearly complete," Ablashi and co-workers reported.
In a third variation of the experiment, cells were not pretreated with Ampligen, but treated only at the time of viral infection; no Ampligen was added thereafter to the cultures. Even under these conditions, there was inhibition of viral replication, ranging from 45.7 to 89.1 percent.
The fourth permutation in this series of experiments was the also quite successful: When the cells were not pre-treated but were treated continuously with Ampligen after HHV-6 infection, there was a "dose related inhibition of virus replication, ranging from 95.5-91.3 percent at three different concentrations (50, 100, and 200 micrograms/milliliter)," Ablashi and colleagues report. A concentration of only ten micrograms/milliliter was not enough to inhibit HHV-6 infection, they found.
Perhaps the best news in this study is that inhibition of HHV-6 with Ampligen resulted in absolutely no toxicity to the cells; they remained "90 percent viable," i.e., alive.3 This study indicates that Ampligen appears not only to stop replication of the virus, but also to stop HHV-6 from maturing once it is in the cell.
But do those effects, in the lab, translate into clinical improvement when people with active HHV-6 infections are treated with Ampligen? In 1995, a study was published that showed long-term improvement in patients with Chronic Fatigue Syndrome who were treated with Ampligen. Ablashi was an investigator in this study, as were Ampligen co-inventor William Carter, CFS researchers Daniel Peterson, David R. Strayer, Robert J. Suhadolnik, Sheila Bastien, HHV-6 researcher Berch Henry, and others.4
The answer to the question of whether Ampligen improved the health of CFS patients, who are known to have active HHV-6 infections, was yes. Improvement was noted in patients' Karnofsky Performance Scale (KPS), a measure of ability to perform daily activities like taking care of oneself; memory and IQ improved; exercise tolerance was increased; and there was a measurable reduction of HHV-6 activity.
The Strayer paper reported not only these marked improvements in CFS patients treated with Ampligen, but that they were sustained over the long term.
Fifteen CFS patients, all of whom met the Centers for Disease Control criteria for CFS, participated in the experiment. Their mean age was 44, and 73 percent were women. These patients had been sick for an average of 33 months. "All 15 patients were functionally impaired by their illness as evidenced by their mean baseline Karnofsky Performance Score of 47 (range 20-60)," Strayer and colleagues reported. A KPS score of 100 is considered normally functional. There were two dose regimens administered to the study participants. Initially, they received 200 milligram of Ampligen intravenously twice a week "for variable periods of time"; then, the dosage was increased to 400 milligrams twice a week. Some patients' doses were increased to 400 milligrams three times a week.
Patients were monitored for active Human Herpes Virus 6 infection by blood cultures, which were "observed periodically for the formation of giant cells characteristic of herpesvirus infection," according to Strayer et al. HHV-6 itself was found in those giant cells, and the percentage of those cells infected with Variant A HHV-6 (the GS strain) was determined.
Some patients had more than ten percent "giant cells" in their cultured blood cells, scored as "two"; those with between 0 percent and ten percent scored as "one"; and those with no giant cells scored as "zero."5
No patient in the study dropped out because of toxicity from the drug. At the beginning of Ampligen therapy, patients reported an increase in flu-like symptoms (muscle and headaches), but those symptoms "typically abated" as treatment continued.
"There were no clinically significant alterations of coagulation, blood chemistry values, white blood counts, or liver and renal function test values throughout the course of this study," Strayer and colleagues reported. "Only two adverse events, one case each of feeling lightheaded and facial flushing, were reported as definitely related to Ampligen. There were no severe adverse events attributed to Ampligen." One patient became anemic because of the amount of blood drawn for testing, and was treated with an iron supplement. There were also changes in laboratory blood test values-red blood cell count, hemoglobin, numbers of different types of lymphocytes and platelets-noted during this study. Blood clotting remained normal, as did urinalysis.
Perhaps the most striking improvement was measured by the Karnofsky Performance score (KPS), as Strayer and co-workers explained: "Patients entering the study were significantly incapacitated, with a mean Karnofsky performance score (KPS) of 47. At a KPS level of 40-50 an individual is significantly disabled and requires special care or considerable assistance to perform normal activities of daily living. Self-care is limited and 50 percent or more of the individual's's waking hours are spent confined to bed and/or chair. The average score improved to 67 after 12 weeks of Ampligen therapy. A KPS score of 60-70 describes an individual able to care for most needs with no or only occasional assistance, but unable to carry out any work activities.
"KPS showed sustained improvements through 60 weeks, reaching 80 by 24 weeks and 85 by 60 weeks. An 80 KPS score describes a person capable of normal activity with effort. Some signs and symptoms of disease are still present but no special care is required. The [statistical analysis performed] strongly suggested that the continued increase in KPS during the first 24 weeks of Ampligen therapy was statistically significant."6
Ampligen also reduced the presence of the giant cells indicative of HHV-6 infection. All 14 patients were positive for giant cells before Ampligen treatment. The number of such cells increased during Ampligen treatment in 50 percent of the patients at eight weeks, and in 77 percent at 16 weeks. Four of the patients actually became culture-negative for HHV-6 during Ampligen treatment. In other words: Ampligen stops HHV-6.
In fact, this not-yet-approved, non-toxic drug appears to inhibit the growth of the "AIDS cofactor" completely.
In addition to the other clinical improvements noted during Ampligen treatment, cognitive functioning also increased. Memory scores increased as much as 23 to 45 percent, as did IQ scores.
Only two of the patients in the study failed to experience all of these improvements in clinical status, for unknown reasons. The clinical effects of Ampligen, like its ability to inhibit HHV-6's growth, appeared to be dose-dependent; the most dramatic improvements in daily functioning, Strayer and co-authors point out, occurred after Ampligen dosage was increased to 400 milligrams.
Strayer and colleagues speculate that these clinical improvements could be associated with Ampligen's inhibition of HHV-6.
"Reduced ability to obtain giant cells in short term culture of blood mononuclear cells was noted during Ampligen treatment," they reported. "In eight cases, giant cells were shown to express HHV-6, utilizing specific monoclonal antibodies. This could have resulted from a restoration of normal lymphokine balance, from direct inhibition of virus replication, or from elimination of HHV-6 expressive cells by immune mechanisms. Giant cell formation in this system is associated with HHV-6 infection, but it is not known whether HHV-6 expression or giant cell formation contributes to CFS symptomatology. However, recent studies show that Ampligen can inhibit in vitro replication of HHV-6...."
Why has this seemingly safe, effective drug not been approved by the FDA?
Is it because a treatment that proves effective for both CFS and AIDS would highlight the connection between the two syndromes? References
  1. Ablashi, D.V. et al.; "Ampligen Inhibits Human Herpesvirus-6 in Vitro"; in vivo 8:587, 1994.
  2. Ibid.
  3. Ablashi et al., op cit.
  4. Strayer, David R. et al.; "Long Term Improvements in Patients With Chronic Fatigue Syndrome Treated With Ampligen"; Journal of Chronic Fatigue Syndrome 1(1):35, 1995.
  5. Ibid.
  6. Strayer et al., op cit

Some of the most interesting statements about Multisystemic HHV-6

"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
"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
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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The Virus Within: A Coming Epidemic

Although Dr. Anthony Fauci, the man in charge of AIDS research in the United States, attended the conference and presented the work his research group had performed on the lymph nodes of AIDS patients, neither he nor any other government scientist chose to comment about the parallel finding about T4 cells in the lymph nodes of AIDS and CFS patients. --Neenyah Ostrom
"HHV-6 has been shown to infect endothelial cells and can establish chronic infection in these cells. . . . The infection of the cells can likely alter function of the endothelial cell and the cell surface, thus leading to activation of the coagulation pathways." --Dr. Joseph Brewer
"In an article in the Journal of Clinical Virology (in press), Dr. Dharam Ablashi, one of the world's leading experts on HHV6, concludes that CFS (ME/CFIDS) patients are acquiring HHV-6A as a primary infection as adults and not reactivating it from childhood as many have hypothesized."
"Until the denial among medical professionals about the relationship between the AIDS and Chronic Fatigue Syndrome epidemics is overcome, however, it is difficult to imagine how either epidemic can be ended." --Neenyah Ostrom America's Biggest Cover-up
"Carrigan and Knox, meanwhile, were pursuing a theory that had been considered, and rejected, by researchers earlier - that HHV-6 might be a "co-factor" in AIDS, aiding and abetting HIV in the destruction of victims' immune functions. Soon, Regush relates, Knox was wondering, "was HIV doing any killing, or was HHV-6 the lone assassin?" But in 1997, after Carrigan and Knox found evidence suggesting HHV-6 might be killing alone, the British medical journal The Lancet rejected their paper for publication." --Mark Nichols
"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."
" . . . 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."
-Konnie Knox
"ICL is 'non-HIV AIDS' or AIDS patients in whom HIV is not present. ICL is almost certainly 'HHV-6 AIDS.' The fact that non-HIV AIDS even exists and is acknowledged should be a major media event, a major medical discovery, and a cause for more research dollars. If the general public knew that non-HIV AIDS existed, much doubt would be cast on medical, governmental, and pharmaceutical company dollars spent on AIDS research. But money does play a role in healthcare that is frightening." --Dennis Gersten, M.D.
"But Dr. Cheney also has CFS patients with very low CD4 cells counts; so low, in fact, that they can be diagnosed as being "non-HIV AIDS," or ICL, cases." --Neenyah Ostrom, America's Biggest Cover-up
"While most researchers have been concerned with HHV-6’s effects on the CNS, recent studies suggest HHV-6 may able to profoundly alter the functioning of the immune system. Rather startlingly it may be able to do so simply by binding to a protein found on the outer membranes of cells." --Cort Johnson
Dr. Dharam Ablashi, co-discoverer of the virus and scientific director of the HHV-6 Foundation said, "There is good reason that it has taken a long time to build a case for this virus playing a role in chronic fatigue -- it's very difficult to find. The virus is 'neurotropic' meaning it prefers to live in the brain tissue. It is quite possible to find a significant infection in the brain tissue, but no virus in the serum by DNA testing." Dr. Daniel Peterson, a leading CFS clinician from Sierra Internal Medicine in Nevada, supported this finding. He performed spinal taps on patients with abnormal MRI or severe problems with cognitive functioning and found active HHV-6A virus in the spinal fluid of 20% of those patients. Twenty nine percent of these patients were positive at least once in the serum, and he found many patients who were positive in the spinal fluid but not the blood. Warned Peterson, "Just because you can't find it in the blood doesn't mean it isn't there."
"It doesn't take a rocket scientist to realize some very important implications here. Major targets of HHV-6 infection are T-cells, neuronal cells of the brain, central, and peripheral nervous systems, and the bone-marrow. Doctors listen up here! Any virus capable of directly infecting and thus altering the function of these types of cells cannot be good for you! Is it any wonder why many of us are so very ill and we are so dysfunctional. It is about time that doctor's take note and find out these critical facts for themselves by checking on the published literature via Medline since the CDC and the NIH certainly aren't going to tell the whole story yet!"
--Alan Cochetto
Thus, AIDS-associated cancers may represent examples of a process of immunosuppression allowing other oncogenic viruses such as EBV or the more recently discovered human herpes virus 6 (HHV-6) to be expressed as cancer (Cohen, 1991). --William A. Blattner, M.D.
Two new studies provide evidence that human herpes virus 6 (HHV-6) plays a role in AIDS-associated retinitis, and may even be a cofactor with HIV in the pathogenesis of AIDS. Anne -Marie Fillet and her colleagues in Paris suspected the presence of "an etiological link between HHV-6 and AIDS- associated retinitis" because of the "ubiquitous nature of HHV -6 and its genomic relationship with cytomegalovirus." They report in the Journal of Medical Virology that HHV-6 was found to be present in three cases of AIDS-associated retinitis, but not in a control group and concluded that "HHV-6 infects the retina but ... does not have an exclusive causative role in AIDS-associated retinitis. Meanwhile, another group of researchers, led by Donald R. Carrigan, report in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology that their research shows that "at the time of autopsy every patient with AIDS has an active infection with HHV-6 in essentially every tissue." The researchers conclude, therefore, that HHV-6A, a particular strain of the virus, is a necessary, but not sufficient, component in the pathogenesis of AIDS.
"HHV-6 is probably the most neurotropic virus known. Neuroinvasion has been documented in infants with primary infection, in focal encephalitis, in children and adults with AIDS, in recipients of bone marrow transplants, as well as in immunologically competent children and adults. Challoner et al. (78) reported viral DNA sequences in approximately two thirds of brain specimens and viral antigen expression in a number of cell types (e.g., astrocytes, macrophages, epithelial cells, endothelial cells of blood vessels) at very similar frequencies in specimens from healthy persons and multiple sclerosis patients. Astrocytes were confirmed as a susceptible cell population, although in a subsequent study only samples from AIDS patients were positive (79)"
"In an article in the Journal of Clinical Virology (in press), Dr. Dharam Ablashi, one of the world's leading experts on HHV6, concludes that CFS (ME/CFIDS) patients are acquiring HHV-6A as a primary infection as adults and not reactivating it from childhood as many have hypothesized. He also found that the infection has been shown to downregulate the central nervous system, the cardiac system, and the cerebral systems. While variant B was found to be the culprit in multiple sclerosis, variant A was doing the damage in CFS and is found in similar numbers as affects those with AIDS (70%). Reporting on his newest discoveries at the New Jersey CFSA Conference, he said, despite prior reports to the contrary, there were no (0%) controls found with the infection of the A strain, although some healthy controls were found to have the B strain. Dr. Ablashi did the work by short-term culturing, PCR or RNA for the PCR, and IGM in antibody serum and plasma and found HHV7 was not found, but there was no doubt about HHV-6A being the culprit in the majority of patients tested."
--Robert Huntington
"The probability that HHV-6 encodes for a miRNA is high at 84%, although no miRNA has been identified yet. Possibly expressed at very low levels, miRNAs derived from HHV-6 may have escaped detection so far."
"... early proteins of HHV-6 infection alter mitochondrial membrane potential." Dr. David Bell in 2008 on research by Dr. L. Flammand
"The epidemic of the acquired immunodeficiency syndrome (AIDS) is in its second decade and continues its worldwide expansion. In some developing countries, more than 20% of all adults are infected with the human immunodeficiency virus (HIV).1 The successful use of multiple antiviral drug therapies has been limited by the complex dosing schedules required and by the emergence of resistant forms of HIV. Work on vaccines to prevent or treat HIV infections continues, but it appears that an effective vaccine is still several years away. Clearly, there exists a need for new strategies in the treatment of HIV disease, especially if these strategies can provide new targets for effective pharmaceutical or immunological therapies. Human herpesvirus six (HHV-6) may serve as an important cofactor in the pathogenesis of AIDS and may provide an alternative target for therapeutic intervention." --Konnie Knox and Donald Carrigan

Gallo on HHV-6

Here's what Robert Gallo had to say about HHV-6 in an NIH interview in 1995:

Have we ever argued for a possible cofactor? Yes, with the qualification I just told you, that it is obvious that some things will promote progression and some things will inhibit progression. One of those things may be the genetics of me versus you. We can say dose is a factor that can lead to progression, or lack of it, and at a greater or lesser rate. But we have argued for certain herpesviruses as possibly being a factor in promoting AIDS progression. Several groups have argued for cytomegalovirus because it does do things and it does activate more HIV in some subtle settings.
In the middle of the 1980s, we became aware that the lymphomas that were associated with HIV infection were perhaps one-third of the time EBV-positive. Epstein-Barr virus, as you know, can immortalize some B cells and, when you have EBV-positive lymphomas, generally they are the kind of lymphomas that, more or less... If they do not require EBV, EBV makes the probability of getting a lymphoma much greater, because the cell cannot die easily. It is immortalized. Other genetic events are needed to develop the lymphoma, but the immortalization of the cell is perhaps a key factor that makes it probable that it will be an EBV-containing cell that is the one that will become a lymphoma.
What about the two-thirds of lymphomas in HIV-infected persons that were not EBV-positive? We wondered if there were herpesviruses yet to be discovered. We looked in the B-cell lymphomas of patients with AIDS who were negative for EBV and we discovered the first new herpesvirus in 25 years, and the first herpesvirus of man that targeted predominantly the T cell.
We had a new herpesvirus, but it was not involved in the lymphoma, at least not as far as anybody knows, even today. We even misnamed it. We called it HBLV, because we found it in a B-cell lymphoma. Then we studied it more intensively and determined that it primarily infected T cells, not B cells, which was an unexpected finding. We learned that it killed T cells when it replicated. Then we learned that it infected natural killer cells and, when it did so, it made those cells attack other natural killer cells. We learned that it could infect the same cell as HIV and activate HIV expression. Next we learned that it infected CD8 cells and activated the gene for CD4, the only known biological agent I am aware of that activates the gene for CD4. Now, the CD4+/CD8+ cells could be targets for HIV.
It was at that stage we proposed that the herpesvirus might be a cofactor for progression of AIDS. It was then that I started to be careful of the use of these words and called it a catalyst for progression, that is, a nonessential cofactor, but something that makes disease progression go faster and also makes it more probable that immune deficiency will develop.
We put that idea out and it got a little bit of a reception by [Dr. Larry] Corey in Seattle, and by [Dr. Donald] Don Carrigan at Wisconsin. But then [Dr. Harold] Jaffe published a paper, the data of which we already had in hand. I think that paper by Jaffe and his colleagues at the CDC [Centers for Disease Control and Prevention] was not a sophisticated look at the problem. Namely, they said, Look, everybody has antibody, so how can it be a factor in progression? That is like saying a cytokine like TNF [tumor necrosis factor] is not important in disease pathogenesis because everybody has it. The question is, if 90 percent of the human population has it, they also have EBV, but EBV can cause Burkitt's lymphoma under certain settings. The question is, does it get activated in an immune-suppressed individual?
We put the problem aside for a while because we did not have a quantitative assay to measure the amount of herpesvirus; only this antibody that indicated a previous exposure to the virus, which everybody showed. We argued, however, when we presented it, that we needed to have a quantitative assay for virus in blood and the amount of human herpesvirus-6 [HHV-6] DNA in lymphocytes circulating around.
At this time we learned of Carrigan's work. He reported in a few clinical papers, that sometimes in immune-suppressed people, following transplantations, he saw an enormous amount of human herpesvirus-6 replication and that he believed it was responsible for some of the bone marrow abnormalities in such people. He showed a lot of virus in bone marrow. Second, he pointed out and emphasized that interstitial pneumonia is the cause of death in 10 percent of the deaths of HIV-positive people. No one knows the cause of that interstitial pneumonia, and he found the lungs of those who died loaded with human HHV-6. He presented at our laboratory meeting that he thought it was very likely that HHV-6 was the cause of those deaths.
Meanwhile, before this, Japanese workers had shown that HHV-6 was the cause of roseola infantum, also known as exanthem subitum, a disease of infants, with fever and rash, but usually with not much more.
So now what is new? I have discussed with my colleague [Dr.] Paolo Russo that the only way we are going to get any proof of this, or get stronger support, is if we get a specific inhibitor that does not inhibit HIV, inhibits HHV-6, and as far as we know does not inhibit anything else, is relatively non-toxic, and then show that patients do better rather than worse.
Another way of doing it would be to find an animal model not infected with a parallel virus to HHV-6 which can be infected by SIV [simian immunodeficiency virus]. SIV can induce some immune deficiency not the acute sort but there are monkeys in which SIV induces nothing, there are monkeys in which some strains of SIV induce an acute AIDS, and there are monkeys where some strains of SIV induce a disease more similar to the human disease, where it takes time.
We used such a system. This is not published data. 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.

Five books that uncover the truth about HHV-6

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The Virus Within: A Coming Epidemic by Nicholas Regush

Neenyah Ostrom's Three Books on Chronic Fatigue Syndrome and HHV-6

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What Really Killed Gilda Radner?: Frontline Reports on the Chronic Fatigue Syndrome Epidemic

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50 Things You Should Know About the Chronic Fatigue Syndrome Epidemic

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America's Biggest Cover-Up: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic And Its Link to AIDS

The first work of fiction about HHV-6 and its political, racial and sexual implications.

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The Closing Argument by Charles Ortleb

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