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Saturday, February 29, 2020

Is HHV-6's Big Day Coming?



"He’s convinced herpesviruses play an important role and that new herpesviruses may be found in the next couple of years."
 http://www.prohealth.com/library/showarticle.cfm?libid=19956




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Some Important Statements about HHV-6


"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

 


Thursday, February 27, 2020

Ampligen, the AIDS and Chronic Fatigue Syndrome drug, is recruited for treating COVID-19



https://www.pressviewer.com/ViewEmail.asp?b=2265&id=187832&p=2173771&I=1243298-K2r3p5x9n5

AIM ImmunoTech Joins with ChinaGoAbroad for an Ampligen China Entry Against COVID-19, the New SARS-like Coronavirus Disease Epidemic
OCALA, FL / ACCESSWIRE / February 27, 2020 / AIM ImmunoTech (NYSE American: AIM, or the Company), an immuno-pharma company focused on the research and development of therapeutics to treat immune disorders, viral diseases and multiple types of cancers, today announced that the Company has joined with ChinaGoAbroad (CGA) to facilitate the entry of AIM's experimental drug Ampligen into the People's Republic of China (PRC) for use as a prophylactic/early-onset therapeutic against COVID-19, the new SARS-like coronavirus infection that has reached epidemic proportions.
CGA is a member-based online information platform and offline advisory firm serving to facilitate two-way international transactions relating to the PRC in close collaboration with the China Overseas Development Association (CODA), which had up until recently reported to the PRC National Development and Reform Commission (NDRC), which in turn reports to the State Council (China's cabinet). CGA is already involved in China's ongoing efforts to halt the growing COVID-19 epidemic and, among other engagements, has been assigned to assist with the international purchase by Sinopharm Group - a Chinese state pharmaceutical company - of technology, masks, gowns and gloves.
"AIM is working aggressively to advance the introduction of Ampligen into China, in order to provide the Chinese people with a potential first line of defense against the deadly COVID-19 virus. AIM and CGA have taken this first step to facilitate discussions with the Chinese government for Ampligen's entry into China as a targeted prophylactic/early-onset therapy," said AIM CEO Thomas K. Equels. "Ampligen achieved a 100% survival rate, as compared to 100% mortality in the untreated control animals, in SARS animal experiments after the outbreak in 2003. In these experiments, Ampligen was administered to mice prior to and shortly after infection. The Company believes that Ampligen may provide similarly effective prophylaxis against COVID-19, as both coronaviruses are extremely similar in key regulatory RNA sequences essential for coronaviral replication."
Ampligen has a well-developed safety profile based on approximately 100,000 IV doses administered to humans and is ready to deploy for clinical trials in China if trials are approved by the PRC authorities and if Ampligen is authorized for export under the FDA regulations governing the export of investigational drugs for use in a sudden and immediate national emergency. (See: "Ampligen as an Antiviral," safety slides 7-15, at https://aimimmuno.com/events-presentations/).
ChinaGoAbroad CEO Jesse T H Chang states: "Ampligen has the potential to be a groundbreaking life-saving protective therapy. This drug may be useful for doctors, nurses, healthcare professionals, first responders and people exposed to the virus. Without better protection, infected professionals in our medical teams may continue to become martyrs on the frontlines of the battle against this highly contagious virus. If Ampligen works in the clinic against COVID-19 the same way it worked in the SARS experiments, a protective drug such as Ampligen - unlike a mask and gloves - would provide immunological protection from the inside. For those inadvertently exposed to the virus, it may provide hope against infection or development of the disease. Such a protective therapy would also become an important public health tool against exposed people spreading the disease. We are excited and indeed honored to work with AIM ImmunoTech on this endeavor so important to the Chinese people."
In addition, you can find AIM's most recent stockholder update detailing Ampligen's potential in the epidemic here: https://aimimmuno.irpass.com/AIM-ImmunoTech-Issues-Stockholder-Update-on-the-Potential-Role-of-Ampligen-for-Use-Against-the-Wuhan-Coronavirus-Epidemic
About AIM ImmunoTech Inc
AIM ImmunoTech Inc. is an immuno-pharma company focused on the research and development of therapeutics to treat immune disorders, viral diseases and multiple types of cancers. AIM's flagship products include the Argentina-approved drug rintatolimod (trade names Ampligen® or Rintamod®) and the FDA-approved drug Alferon N Injection®. Based on results of published, peer-reviewed pre-clinical studies and clinical trials, AIM believes that Ampligen® may have broad-spectrum anti-viral and anti-cancer properties. Clinical trials of Ampligen® include studies of cancer patients with renal cell carcinoma, malignant melanoma, colorectal cancer, advanced recurrent ovarian cancer and triple negative metastatic breast cancer. These and other potential uses will require additional clinical trials to confirm the safety and effectiveness data necessary to support regulatory approval and additional funding. Rintatolimod is a double-stranded RNA being developed for globally important debilitating diseases and disorders of the immune system.
Cautionary Statement
This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "may," "will," "expect," "plan," "anticipate" and similar expressions (as well as other words or expressions referencing future events or circumstances) are intended to identify forward-looking statements. These statements involve a number of risks and uncertainties. For example, significant additional testing and trials will be required to determine whether Ampligen will be effective in the treatment of the Wuhan Coronavirus in humans and no assurance can be given that it will be the case. The presentation and stockholders' letter referenced in this press release refer to a number of studies. No assurance can be given that future studies will not result in findings that are different from those reported in the referenced studies. This press release related to potential activity in China. Operating in foreign countries such as China carries with it a number of risks, including potential difficulties in enforcing intellectual property rights. We cannot assure that our potential operations in China will not be adversely affected by these risks. With regard to the Company's activities with Ampligen generally, no assurance can be given as to whether current or planned trials will be successful or yield favorable data and the trials are subject to many factors including lack of regulatory approval(s), lack of study drug, or a change in priorities at the institutions sponsoring other trials. In addition, initiation of planned clinical trials may not occur secondary to many factors including lack of regulatory approval(s) or lack of study drug. Even if these clinical trials are initiated, the Company cannot assure that the clinical studies will be successful or yield any useful data or require additional funding. Any forward-looking statements set forth herein speak only as of the date of this press release. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. The information found on our website is not incorporated by reference herein and is included for reference purposes only.
Contacts:
Crescendo Communications, LLC
Phone: 212-671-1021
Email: aim@crescendo-ir.com
AIM ImmunoTech Inc
Phone: 800-778-4042
Email: IR@aimimmuno.com
SOURCE: AIM ImmunoTech Inc


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https://www.accesswire.com/578078/AIM-ImmunoTech-Joins-with-ChinaGoAbroad-for-an-Ampligen-China-Entry-Against-COVID-19-the-New-SARS-like-Coronavirus-Disease-Epidemic

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2/27/2020 10:05:52 AM1243298

Saturday, February 22, 2020

Why has the Chronic Fatigue Syndrome community chosen to ignore this statement from the University of Wurzburg?

From the University of Wurzburg:


"While HHV-6 was long believed to have no negative impact on human health, scientists today increasingly suspect the virus of causing various diseases such as multiple sclerosis or chronic fatigue syndrome. Recent studies even suggest that HHV-6 might play a role in the pathogenesis of several diseases of the central nervous system such as schizophrenia, bipolar disorder, depression or Alzheimer's."



The scientist who deserves a Nobel Prize for his work on HHV-6 and Chronic Fatigue Syndrome.


https://www.uni-wuerzburg.de/en/news-and-events/news/detail/news/viruses-under-the-microscope/


Viruses Under the Microscope


09/14/2018
Human herpesviruses such as HHV-6 can remain dormant in cells for many years without being noticed. When reactivated, they can cause serious clinical conditions. Researchers from Würzburg have now found a way of differentiating between active and inactive viruses. 





Human herpesvirus 6 (HHV-6) infects almost all of the human population, but only very few will show any symptoms during their lifetime: HHV-6 is one of the most widespread viruses among the population. Between 95 and 100 percent of healthy adults have antibodies to the virus which means that they have been infected at some point in the past.

The virus hides in the genomic DNA

There are two types of the virus: HHV-6A and HHV-6B. HHV-6B primarily infects in infancy as sixth disease, whereas HHV-6A infections usually remain asymptomatic. After primary infection, the virus establishes lifelong latency by integrating with the cellular DNA.
The infection is generally harmless. Under certain circumstances, however, the virus can be reactivated – for example, after chlamydia infection, organ transplantation, immunodeficiency or when taking specific drugs. 

Trigger of numerous diseases

While HHV-6 was long believed to have no negative impact on human health, scientists today increasingly suspect the virus of causing various diseases such as multiple sclerosis or chronic fatigue syndrome. Recent studies even suggest that HHV-6 might play a role in the pathogenesis of several diseases of the central nervous system such as schizophrenia, bipolar disorder, depression or Alzheimer's.
Dr. Bhupesh Prusty is responsible for these new insights. The scientist is a team leader at the Department of Microbiology of the University of Würzburg. Prusty has recently discovered a method which for the first time allows reactivation of human herpesvirus to be detected at an early stage.

MicroRNA molecules as markers

"Betaherpesviruses like human herpesvirus 6A, 6B and 7 integrate into subtelomeric ends of human chromosomes and acquire latency. This makes it difficult to recognize the early phase of viral activation based on an analysis of the viral DNA," Prusty points out the problem. Together with his team, the virologist has now discovered an alternative approach which could be a suitable biomarker for HHV-6 studies.
"We have identified several viral microRNA molecules which are produced both during active infection and viral activation," Prusty explains. MicroRNAs directly influence cell metabolism. The RNA assures the flow of genetic information from nuclear DNA into the cell where it is "translated" to proteins. The microRNAs have a regulatory function in this process. They can dock to RNA molecules and prevent them from being translated to proteins or initiate the degradation of RNA molecules. Prusty is certain that the detection of these viral microRNAs can serve as an ideal biomarker under clinical conditions.

Biopsies confirm hypothesis

The scientists were able to confirm their hypothesis by studying biopsies of a young woman who had died tragically as a result of drug-induced hypersensitivity syndrome (DRESS), a usually life-threatening condition which results in rash, organ failure and blood count anomalies.
Scientists have suspected for some time that these cases might have been caused by drugs that activate viruses but were unable to provide evidence for this theory. Prusty and his colleagues have now detected traces of HHV-6 DNA in the blood of the deceased – however different concentrations at various stages of the disease. At the time of death, for example, the viral load was very low while the opposite was true for the concentration of microRNA: "All biopsy samples showed a positive signal for this special type of RNA," Bhupesh Prusty says. This indicates the potential effectiveness of RNA as a viral biomarker for the detection of active viral infection in the body.
With this finding, Prusty and his team have demonstrated for the first time in experiments that some of the prescription drugs have the potential to reactivate HHV-6 with life-threatening consequences. Early detection of viral reactivation may therefore be helpful for further clinical interventions.

Bhupesh Prusty earns Young Investigator Award for Excellence in Basic Science



Dr. Bhupesh Prusty and Professor Thomas


Rudel Discuss their Research 




"Brupesh Prusty is determining if HHV-6 infections are hampering mitochondrial functioning in ME/CFS."
https://www.prohealth.com/library/montreal-cfs-metabolism-main-matter-81052

HHV-6 Mediated Mitochondrial Modulation and Its Association to ME/CFs
A project summary as written by Bhupesh Prusty:



Infections are frequently associated with chronic disease development and likely, play crucial roles in the onset or progression of several human disorders that are not classified as infectious diseases.Myalgic encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) is one such example. However, the precise role of pathogens in ME/CFS development remains, predominantly, uncharacterized. Human Herpesvirus 6 (HHV-6) is frequently associated with several human diseases including ME/CFS. Work from my laboratory as well as from others have shown that HHV-6 frequently integrates into human chromosomes in order to achieve latency (ciHHV-6). Originally, ciHHV-6 was thought to be the dead end for the virus. However recent publications demonstrate that certain timely triggers like circumstances of immune suppression or influence of various drugs and/or pathogenic infections can activate the integrated virus.



Our preliminary work shows that HHV-6 targets the cell’s energy reserve, the mitochondria, during

both active infection and activation from latency leading to mitochondrial dysfunction, a condition that is also frequently associated with ME/CFS. Using a unique latent and chromosomally integrated

HHV-6 cell culture model, we have observed down regulation of a small non-coding human microRNA in response to viral infection that induces expression of tumor suppressor protein p53 and subsequently that of Drp1 leading to mitochondrial fragmentation. Because of these events,

mitochondria from the infected cells tend to have lower ATP generation capacity and reduced

efficiency for maintaining calcium homeostasis. In this proposal, we aim to dissect out the contributing factor from HHV-6 that is directly responsible for the signaling processes leading to host cell mitochondrial alteration. We have identified several viral miRNAs that are specifically expressed during both active infection and viral activation. We hypothesize that these viral miRNAs play a key role in alteration of mitochondrial fission-fusion dynamics. Our final aim is to link HHV-6 and mitochondrial alterations using ME/CFS patient materials. Molecular mechanisms behind direct

association between HHV-6 and human mitochondria have never been studied before. The proposed project aims to elucidate the molecular mechanism(s) by which HHV-6 infection actuates mitochondrial dysfunction in ME/CFS patients, likely, resulting in the development/progression of ME/CFS.



The anticipated outcome of this pioneering research idea is the elucidation of a novel infectioninduced mechanism for the onset and/or progression of ME/CFS. Understanding etiology of mitochondrial modulation from thus far unknown causative agents will open new targets for drug

development. Infectious agents behind mitochondrial modulation in ME/CFS are poorly characterized and the proposed research aims to address this unexplored avenue. The idea that a common virus like HHV-6 could associate with host cell mitochondria and modulate its function (and contribute to disease) has not been hypothesized before. I believe that my project has tremendous potential to revolutionize the preconceived theories about pathogenic causes behind ME/CFS and is in line with the Solve ME/CFS Initiative’s mission as well as funding objectives.



Has Bhupesh Prusty found an effective treatment for HHV-6 and Chronic Fatigue Syndrome?

Anti-herpesviral effects of a novel broad range anti-microbial quaternary ammonium silane, K21
by Nitish Gulve, Bhupesh K Prusty, Dharam Ablashi, and Gerhard Krueger

We have created a novel quaternary ammonium silane, K21 through sol-gel chemistry, using an ethoxylated version of an organosilane quaternary ammonium compound and TetraEthyl Ortho Silicate (TEOS) as precursors. Previous studies using the precursor molecule quaternary ammonium compounds (QACs) and a methacryloxy version of K21, primarily designed for use in dental healthcare, have shown inhibited growth properties against several types of gram-positive and gram-negative bacteria including Escherichia coli, Streptococcus mutans, Actinomyces naeslundii and Candida albicans etc. Here we tested the effect of K21 on HSV-1, HHV-6A and HHV-7 in in vitro cell culture infection models. Our results show growth inhibitory effect of K21 on HSV-1, HHV-6A and HHV-7 infection.


Team 5 – The Potential Role of HHV-6 in ME/CFS


Imbalanced Oxidative Stress Causes Chlamydial Persistence during Non-Productive Human Herpes Virus Co-Infection



Abstract


Both human herpes viruses and Chlamydia are highly prevalent in the human population and are detected together in different human disorders. Here, we demonstrate that co-infection with human herpes virus 6 (HHV6) interferes with the developmental cycle of C. trachomatis and induces persistence. Induction of chlamydial persistence by HHV6 is independent of productive virus infection, but requires the interaction and uptake of the virus by the host cell. On the other hand, viral uptake is strongly promoted under co-infection conditions. Host cell glutathione reductase activity was suppressed by HHV6 causing NADPH accumulation, decreased formation of reduced glutathione and increased oxidative stress. Prevention of oxidative stress restored infectivity of Chlamydia after HHV6-induced persistence. We show that co-infection with Herpes simplex virus 1 or human Cytomegalovirus also induces chlamydial persistence by a similar mechanism suggesting that Chlamydia -human herpes virus co-infections are evolutionary shaped interactions with a thus far unrecognized broad significance.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047427

Powerful forces in the Chronic Fatigue Syndrome community are supporting Bhupesh Prusty. Go to 1:52 on this video:




Science Daily on Bhupesh Prusty

"Purkinje cells are a central part of the human cerebellum, the part of the brain that plays an important role in motor learning, fine motor control of the muscle, equilibrium and posture but also influences emotions, perception, memory and language.
Scientists from the Institute for Virology and Immunobiology of the University of Würzburg and their US colleagues have now made a surprising discovery in these nerve cells. They found a high infection rate of Purkinje neurons with the human herpesvirus HHV-6 for the first time in patients with bipolar disorder and/or severe depression. The study was led by Dr. Bhupesh Prusty, group leader at the Department of Microbiology. The scientists have now published the results of their study in the journal Frontiers in Microbiology."



Cort Johnson on Bhupesh Prusty and HHV-6:

"HHV-6 Infections Whacking ME/CFS Patients Energy? (HHV-6 Mediated Mitochondrial Modulation and Its Association to ME/CFS)
After a long period in which HHV-6 infection hasn’t been addressed much in ME/CFS, the bug is showing life again. At the last IACFS/ME conference Nancy Klimas showed (unpublished) that indices of HHV-6 activation are correlated with symptom severity in ME/CFS. Now, working off of their lab’s findings showing that HHV-6 can affect mitochondrial functioning.
Bhupesh Prusty will determine just how this is happening and how often it’s happening in ME/CFS. If it turns out this ubiquitous pathogen – found in almost everyone – is sapping the cells’ energy – that would, of course, really be something."






Read the definitive book on the history of HHV-6 in Chronic Fatigue Syndrome.



On April 16, 1996, Congressman Jerrold Nadler spoke on the floor of Congress about his request for a General Accounting investigation into how the CDC had handled the Chronic Fatigue Syndrome epidemic. Nadler did that at the urging of Charles Ortleb, the publisher and the New York Native and his reporter Neenyah Ostrom. Ortleb and Ostrom had made the case to Nadler that Chronic Fatigue Syndrome and the virus it had been linked to, HHV-6, were serious public health issues.         
                                      
In an interview in New York Native with Neenyah Ostrom, Congressman Nadler said, "Congress can mandate research into CFS as a viral disease. Maybe it will turn out that HHV-6A is the cause of CFS; maybe it will turn out that other viruses are involved. But Congress can mandate research into CFS as a contagious, viral disease. I will certainly try to get Congress to do that as soon as possible."

Unfortunately, back in 1996, Nadler's warning to Congress and the medical establishment fell on deaf ears. But now that the Democrats have regained power in the House of Representatives, the newly prominent Congressman Nadler may finally be able to bring the Chronic Fatigue Syndrome epidemic and HHV-6 to the public's attention.

This book by Charles Ortleb, which details Neenyah Ostrom's diligent reporting on Chronic Fatigue Syndrome, is necessary reading for anyone who wants to know the whole history of an epidemic which has been hidden in plain sight. For a decade, starting in 1988, Ostrom reported on Chronic Fatigue Syndrome and the damage that the virus HHV-6 does to patients. What her reporting uncovered about the true nature of the Chronic Fatigue Syndrome epidemic will shock you. 

In The Chronic Fatigue Syndrome Epidemic Cover-up, Charles Ortleb recounts his newspaper's fascinating struggle to get the medical and political establishment to pay attention to Ostrom's pioneering investigative reporting on Chronic Fatigue Syndrome. 

By the time you finish Ortleb's stunning memoir, you will understand why the CDC has been unwilling to tell the public the truth about Chronic Fatigue Syndrome. The CDC does not want the public to know that Chronic Fatigue Syndrome is a transmissible illness linked to a virus that affects every system in the body. They have covered up the illness for so many decades that the neglected virus is totally out of control. Now it is causing a long list of other illnesses and many cancers. The CDC has put us all in danger.

Ostrom's decade of reporting on HHV-6 was recently vindicated by this statement from scientists at the University of Wurzburg:"While HHV-6 was long believed to have no negative impact on human health, scientists today increasingly suspect the virus of causing various diseases such as multiple sclerosis or chronic fatigue syndrome. Recent studies even suggest that HHV-6 might play a role in the pathogenesis of several diseases of the central nervous system such as schizophrenia, bipolar disorder, depression or Alzheimer's." 

The big question about Neenyah Ostrom and New York Native is this: How many lives would have been saved if the scientific establishment and the mainstream media had paid more attention to Neenyah Ostrom's reporting on HHV-6 and Chronic Fatigue Syndrome in New York Native?             

One day, if there is any justice in the world, the CDC and the medical establishment will apologize for not paying attention to Neenyah Ostrom's groundbreaking work on Chronic Fatigue Syndrome that Charles Ortleb published in New York Native. That would be a fitting end to one of journalism's greatest David and Goliath stories.  

  
Anyone who wants to help Congressman Nadler and the other members of Congress who are trying to end the suffering of millions of people with Chronic Fatigue Syndrome, needs to read The Chronic Fatigue Syndrome Epidemic Cover-up.

























Spotify podcasts about the HHV-6 and Chronic Fatigue Syndrome cover-up 




Three Big Books

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Everyone needs to know what the CDC is hiding about CFS and HHV-6. NEW YORK NATIVE contains both volumes of THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP. The print version is $23. Only $7.98 in Kindle.

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