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Monday, January 21, 2019

The bestseller about Chronic Fatigue Syndrome that is waking the world up to an epidemic that threatens everyone.





Available now at Amazon in hardcover, print, Kindle, and Kindle Unlimited.

Mast Cell Activation may be another clue that Chronic Fatigue Syndrome involves Kaposi's Sarcoma.



Mast Cell Activation and KSHV Infection in Kaposi Sarcoma

http://clincancerres.aacrjournals.org/content/24/20/5085

Mast Cell Activation May Underlie 'Chronic Fatigue Syndrome

https://www.medscape.com/viewarticle/893858


Could the Brain’s Mast Cells Be Causing Chronic Fatigue Syndrome (ME/CFS)?


http://simmaronresearch.com/2018/09/brains-mast-cells-causing-chronic-fatigue-syndrome-mecfs/


"Persons infected with KSHV can asymptomatically shed the virus. It is advised to practice safe sex with infected individuals and curtail activities where saliva might be shared during sexual activity."


http://www.herpes.com/hhv-8.html




This is what oral Kaposi's Sarcoma looks like.




Source: https://doctorspiller.com/kaposis-sarcoma/

Compare it to these crimson crescent lesions in the mouths of Chronic Fatigue Syndrome patients.



"Burke A. Cunha, MD, discovered what he called crimson crescents in the mouths of 80% of his CFS patients. After the word got out, Cunha received calls from other parts of the country. Physicians began telling him that they also were finding the crimson crescents in their patients once they looked for them."

https://www.prohealth.com/library/crimson-crescents-facilitate-chronic-fatigue-syndrome-cfs-diagnosis-11266




Chronic Fatigue Syndrome patients may have undiagnosed internal Kaposi's Sarcoma. Susan Levine found HHV-8, the Kaposi's Sarcoma virus, in half of CFS patients she looked at.

Prevalence in the Cerebrospinal Fluid of the Following Infectious Agents in a Cohort of 12 CFS Subjects


Susan Levine

Published online: 04 Dec 2011



Over the last decade a wide variety of infectious agents has been associated with the chronic fatigue syndrome (CFS) as potential etiologies for this disorder by researchers from all over the world. Many of these agents are neurotrophic and have been linked previously to other diseases involving the central nervous system (CNS). Human herpes virus-6 (HHV-6), especially the B variant, has been found in autopsy specimens of patients who suffered from multiple sclerosis. Because patients with CFS manifest a wide range of symptoms involving the CNS as shown by abnormalities on brain MRIs, SPECT scans of the brain and results of tilt table testing we sought to determine the prevalence of HHV-6, HHV-8, Epstein-Barr virus (EBV), cytomegalovirus (CMV), Mycoplasma species, Chlamydia species, and Coxsackie virus in the spinal fluid of a group of 12 patients with CFS. Although we intended to search mainly for evidence of actively replicating HHV-6, a virus that has been associated by several researchers with this disorder, we found evidence of HHV-8, Chlamydia species, CMV and Coxsackie virus in 6/12 samples. Attempts were made to correlate the clinical presentations of each of these patients, especially the neurological exams and results of objective testing of the CNS, with the particular infectious agent isolated. It was also surprising to obtain such a relatively high yield of infectious agents on cell free specimens of spinal fluid that had not been centrifuged. Future research in spinal fluid analysis, in addition to testing tissue samples by polymerase chain reaction (PCR) and other direct viral isolation techniques will be important in characterizing subpopulations of CFS patients, especially those with involvement of the CNS.

https://www.tandfonline.com/doi/abs/10.1300/J092v09n01_05








Everything you wanted to know about Kaposi’s Sarcoma in Chronic Fatigue Syndrome patients and the growing CFS epidemic of HHV-8, one of the two or three viruses that may be causing Kaposi’s Sarcoma.







Excerpted from The Chronic Fatigue Syndrome Epidemic Cover-up, a bestseller on Amazon.



     Neenyah Ostrom began one of my favorite series of articles in the same issue. Titled “The Color Purple,” Ostrom reported, “Burke Cunha, M.D. who is chief of infectious disease at Winthrop-University Hospital (Mineola, Long Island), has described what he calls ‘crimson crescents’ that appear in the throats of more than 80 percent of chronic fatigue syndrome (CFS) patients. Cunha describes the crescents not only as ‘crimson,’ but ‘purplish.’ The reddish-purplish regions found in CFS patients’ throats sounded quite similar to KS (Kaposi’s sarcoma) in the throat, commented an ‘AIDS’ doctor [who wished to remain anonymous] to whom they were described. Is it possible that the crimson crescents observed in the throats of CFS patients are actually a type of KS?”      Ostrom raised the possibility that the lesions in the throats of CFS patients connected them to the theory that Florida researchers held about KS being the unrecognized but unifying central pathological event AIDS. As I previously reported, the Florida team, headed by Dr. George Hensley, had turned the AIDS paradigm upside down, by finding KS in nearly 100% of AIDS patients, when they explored the internal organs closely during autopsies of AIDS patients. Their fascinating work suggested that KS preceded AIDS and caused more of the immune problem in AIDS than previously thought.

     Basically, Ostrom was asking if the KS-like lesions, in the tonsils of [CFS]patients, were an indication that some kind of unrecognized indolent KS was present internally, something that physicians would not even be thinking about because of the conceptual wall that socially hostile epidemiology had built between AIDS and chronic fatigue syndrome. And the CFS patients were not particularly interested in finding out if they shared KS with AIDS patients.

    Ostrom went even further, in the July 20 issue, and speculated that the dramatic digestive problems in chronic fatigue syndrome were actually the result of the unrecognized chronic or slowly progressive KS in the CFS patients’ digestive tracts. Ostrom noted that Dr. Carol Jessop, who was talking to a group of patients at a chronic fatigue syndrome conference, said, “Almost all patients would say to me, ‘I was totally well until I got this [chronic fatigue syndrome],’ and yet, when I took their past medical histories, I found it wasn’t quite true. Now these aren’t disastrous problems. In fact, if they had gone to their physicians for any of these problems such as irritable bowel, diarrhea and constipation, abdominal cramping, bloating, flatulence, chronic constipation, heartburn, etc., their physician would probably just say, ‘Oh, take this’ and that would be it. So we as physicians didn’t relate to our patients that this was a problem, so they considered themselves to be totally healthy. Yet, if you look at the numbers, 89 percent of the [chronic fatigue syndrome] patients had irritable bowel syndrome, diarrhea alternating with constipation, and abdominal cramping pain episodically. Another 80 percent complained of constant gas, bloating and flatulence. It’s amazing that we can all meet in this room together.”       Ostrom wondered if “Jessop may have uncovered a fallacy in the prevailing wisdom of chronic fatigue syndrome: that it begins as a respiratory, flu-like illness. Instead, as she points out, it may be a digestive tract disturbance. Jessop’s statistic—that more than 80 percent of CFS patients complain of irritable bowel syndrome, abdominal pain, gas, bloating, etc.—corresponds to the more than 80 percent of CFS patients who exhibit a red-to-purplish crescent-shaped lesion in their throats. (Helot, Paul, in the New York Times Long Island edition, January 14, 1992) . . . What if the digestive problems described by the CFS patients are actually caused by KS in the gastrointestinal tract? According to the AIDS Treatment News, ‘The most common HIV-related causes of gastric symptoms include KS, lymphoma, and CMV [cytomegalovirus].’ And while KS is unusual in the esophagus, it ‘may occasionally be found there.’ KS also can cause colitis and diarrhea . . . in people with AIDS.” Ostrom noted, “Gastrointestinal symptoms, it is realized in retrospect, were among the first signs of the ‘AIDS’ epidemic; and, it now seems, were also among the first symptoms seen in the CFS epidemic. That observation raises what should be a relatively simple question to answer: Are the gastrointestinal symptoms in both patient populations caused, in part, by undetected KS?”





Excerpted from The Chronic Fatigue Syndrome Epidemic Cover-up, a bestseller on Amazon.







Important information about the Kaposi’s Sarcoma problem in Chronic Fatigue Syndrome

Whatever happened to the concern about controlling the Kaposi's Sarcoma Virus? What about all the infected Chronic Fatigue Syndrome patients?


Is Kaposi's Sarcoma responsible for the digestive disorders in Chronic Fatigue Syndrome?


HHV-8 is a Kaposi's Sarcoma cancer virus in many AIDS and Chronic Fatigue Syndrome patients and is spread by kissing but the CDC couldn't care less.


Company founded by Robert Gallo suggests 65% of gay men are infected with Kaposi's Sarcoma virus.


Coagulation issues may link Chronic Fatigue Syndrome, Kaposi's Sarcoma, and AIDS


Should Chronic Fatigue Syndrome be added to the spectrum of Kaposi's Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases?


Why Susan Levine may have done the world's most important research on Chronic Fatigue Syndrome.


Does HHV-8 viral load raise questions about the legitimacy of HIV viral load?


Can Chronic Fatigue Syndrome patients with internal Kaposi's Sarcoma pass it on to their partners?


Can most of the symptoms of Chronic Fatigue Syndrome described by Paul Cheney be attributed to internal Kaposi's Sarcoma?


Is Chronic Fatigue Syndrome Associated Kaposi's Sarcoma  (CFSKS) a diagnosis all doctors should become aware of?


Stanford University and Open Medicine Foundation should have a conference on diagnosing Kaposi's Sarcoma in Chronic Fatigue Syndrome.


Why are doctors not looking for Kaposi's Sarcoma in Chronic Fatigue Syndrome patients?


If Chronic Fatigue Syndrome involves HHV-8 and Kaposi's Sarcoma, scientists will have to ask if it came from pigs.


Does the Red Blood Cell Deformability Issue Link Chronic Fatigue Syndrome to Kaposi's Sarcoma and AIDS?


Will the Montoya cytokine study show that Chronic Fatigue Syndrome is Kaposi's Sarcoma Inflammatory Syndrome?


Is Chronic Fatigue Syndrome a Kaposi's Sarcoma inflammatory cytokine syndrome?


How Kaposi's Sarcoma almost undermined the HIV theory of AIDS


How did 50% of Chronic Fatigue Syndrome patients become infected with a Kaposi’s Sarcoma cancer virus?


Has the moment finally come to address the issue of Kaposi's Sarcoma in Chronic Fatigue Syndrome?


Oral Kaposi's Sarcoma looks like the Crimson Crescents in Chronic Fatigue Syndrome patients.


Were oral crimson crescents the first obvious sign of Kaposi's Sarcoma in Chronic Fatigue Syndrome patients?


Did Paul Cheney ever consider the possibility that Chronic Fatigue Syndrome patients have internal Kaposi's Sarcoma?


Is the red blood cell deformability issue another clue that Chronic Fatigue Syndrome is also a Kaposi's Sarcoma Syndrome?


Why is nobody warned about exposure to HHV-8, the Kaposi's Sarcoma virus that even patients with Chronic Fatigue Syndrome are sometimes infected with?


Do petechiae in Chronic Fatigue Syndrome connect it to Kaposi's Sarcoma, HHV-8, and AIDS?


Whatever is causing Kaposi's Sarcoma may be the real cause of Chronic Fatigue Syndrome and AIDS.


A massive epidemic of Kaposi's Sarcoma may be coming.


When Kaposi's Sarcoma almost turned AIDS upside down.


Human herpesvirus 6 activates lytic cycle replication of Kaposi's sarcoma-associated herpesvirus.


All AIDS patients have some form of Kaposi's Sarcoma in this study. Is the same true for Chronic Fatigue Syndrome?


Crimson crescents may suggest that all Chronic Fatigue Syndrome patients have Kaposi's Sarcoma.


Do all Chronic Fatigue Syndrome patients have an indolent form of Kaposi's Sarcoma?


Are these marks on the skin a sign of Kaposi’s Sarcoma in Chronic Fatigue Syndrome?


On autopsy, do the inflamed ganglia of Chronic Fatigue Syndrome patients resemble Kaposi's Sarcoma?


What people don't know about Kaposi's Sarcoma in Chronic Fatigue Syndrome and AIDS.


Do all Chronic Fatigue Syndrome patients show internal Kaposi's Sarcoma upon autopsy?




Decades ago, a New York newspaper sounded the alarm about Kaposi’s Sarcoma in Chronic Fatigue Syndrome. The book about that newspaper is now a must-read bestseller on Amazon. Purchase a hardcover, paperback, or Kindle version here.






Why is the Chronic Fatigue Syndrome community ignoring the biggest breakthrough?

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.

























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