Has Bhupesh Prusty found a promising 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.

http://www.academia.edu/25761322/Anti-herpesviral_effects_of_a_novel_broad_range_anti-microbial_quaternary_ammonium_silane_K21

Will Bhupesh Prusty win a Nobel Prize for clarifying the role of HHV-6 in Chronic Fatigue Syndrome?


"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."

https://www.sciencedaily.com/releases/2018/08/180809112440.htm

Bhupesh Prusty: "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.


Cort Johnson on 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."




New research points to HHV-6 as the cause of mitochondrial dysfunction in Chronic Fatigue Syndrome.

Go to 1:52 on this video:





If you have Amazon Prime or Kindle Unlimited you can immediately begin reading this book.


If you have Amazon Prime or Kindle Unlimited, you can immediately begin reading The Chronic Fatigue Syndrome Epidemic Cover-up and you will soon understand why the facts about the Chronic Fatigue Syndrome epidemic have been hidden from the public for almost four decades.









This is the book causing heated debates about Chronic Fatigue Syndrome and HHV-6, "The Fifty Shades of AIDS Virus," in laboratories, doctor's offices, and homes all over the world.

                                                              


In his bestselling book, The Black Swan, Nassim Nicholas Taleb wrote, "I see the risks of a very strange acute virus spreading throughout the planet." This book by Charles Ortleb warns that the virus causing Chronic Fatigue Syndrome is that virus.

This book belongs in the library of anyone who wants to know the disturbing history of the Chronic Fatigue Syndrome epidemic and the deadly virus HHV-6. Why have the CDC and NIH pretended that the communicable disease fraudulently called "Chronic Fatigue Syndrome" is a mystery for over three decades? By the end of this book of inconvenient truths the answer is crystal clear. The shocking news and bold analysis in this page-turner could lead to a revolution in the science and politics of Chronic Fatigue Syndrome, fibromyalgia, AIDS, autism, and many other illnesses. Scientists, doctors, nurses, patients, journalists, politicians, and historians must begin their journey to a full understanding of the Chronic Fatigue Syndrome epidemic with this book.

As the publisher and editor-in-chief of a small newspaper in New York, Charles Ortleb was the first journalist to devote a publication to uncovering the truth about Chronic Fatigue Syndrome. He assigned Neenyah Ostrom the duty of following every twist and turn of the Chronic Fatigue Syndrome story. No newspaper in the world did more to warn the world about the virus which seems to be triggering Chronic Fatigue Syndrome and many other immunological disorders. Chronic Fatigue Syndrome and AIDS are just the tip of the HHV-6 iceberg.

This provocative book will end the injustice of the silent treatment Neenyah Ostrom's reporting has been getting from the media and The Chronic Fatigue Syndrome community. Ostrom blew the lid off one of the biggest medical secrets of our time: the link between the Chronic Fatigue Syndrome epidemic and AIDS.

Ostrom interviewed most of the major researchers in the field, as well as countless patients and government scientists. She uncovered so many similarities between Chronic Fatigue Syndrome and AIDS that she came to the conclusion that they are part of the same epidemic, and she argued that until their connection is admitted by top government researchers, there is little hope of making real progress in the fight against Chronic Fatigue Syndrome.

Charles Ortleb's book captures all the challenges and excitement of running a small newspaper that was publishing a brilliant journalist who essentially was the Woodward and Bernstein of the Chronic Fatigue Syndrome epidemic. In Rolling Stone, David Black said Ortleb's newspaper deserved a Pulitzer Prize. Randy Shilts praised Ortleb's newspaper in And the Band Played On.

                                                            


This book continues the work Ortleb has been doing to raise awareness about HHV-6 and Chronic Fatigue Syndrome at his website HHV-6 University. Fewer and fewer people now pretend that HHV-6 is harmless. Thanks to Ortleb's efforts, more and more people are abandoning HHV-6 denialism and admitting the virus is at the center of a public health disaster.

 Hillary Johnson, the author of Osler's Web, called it "A rollicking, fascinating and important memoir."














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