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Sunday, July 14, 2019

Evidence piles up that HHV-6 (the AIDS and Chronic Fatigue Syndrome virus) is causing Alzheimer's


Lavinia Alberi Auber, University of Fribourg, Switzerland, probed the olfactory system for signs of HHV-6. Auber studies age-related decline in olfaction, a non-specific harbinger of future AD, PD, or dementia with Lewy bodies (DLB). Auber has seen neuropathological changes that may underlie this gradual loss. Studying postmortem olfactory tissue from 38 people who had symptoms ranging from mild cognitive impairment to severe AD, Auber noticed a prominent and progressive tauopathy in olfactory neurons. She also detected a weak amyloid pathology in the synaptic terminal in the olfactory bulb that looked to her like intracellular amyloid deposits. These could be a response to nerve damage or infection, she believes.

Using immunohistochemistry, Auber also detected certain viral proteins, which indicate a new infection or viral reactivation, only in AD patients. In people with early AD, these antigens were limited to a few neurons. In more advanced cases, staining appeared as puncta scattered across the whole olfactory tract, and co-localized with phosphorylated tau. One synapse away, in the olfactory region of the entorhinal cortex, the viral antigens co-localized with amyloid plaques. In several autopsy cases, she found neurons and microglia that tested positive for HHV6A scattered throughout the entorhinal cortex. 

The results suggest that HHV-6A, and -6B, may spread from the nose through the olfactory circuit into the brain. It remains to be seen if this contributes to, or is an effect of AD progression in these patients. One complication of the study is that herpesviruses can reactivate after death, and Auber agreed that post-mortem delay may have precipitated this in some samples. The work needs to be confirmed and replicated in more subjects, she said.

Conveniently, olfactory neurons can be biopsied in living people. Auber would like to do this to screen for HHV-6 infection. She is evaluating saliva as a less invasive source for detection of specific viruses, and for monitoring changes in the saliva microbiome over the course of Alzheimer’s disease.
Source: Herpesvirus: Trigger for Many Brain Pathologies?

Bhupesh Prusty has vindicated a newspaper that warned the world about HHV-6 in 1986

Bhupesh Prusty was the star at the recent NIH Chronic Fatigue Syndrome conference.

Meeting Agenda:

Thanks to Bhupesh Prusty, the search for the cause of Chronic Fatigue Syndrome may soon be over.

Has Bhupesh Prusty found a promising treatment for HHV-6 and Chronic Fatigue Syndrome?

The Chronic Fatigue Syndrome and HHV-6 Scientist of the Year 

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

Will Bhupesh Prusty add more evidence that HHV-6 is the cause of Chronic Fatigue Syndrome?

"Bhupesh Prusty is determining if HHV-6 infections are hampering mitochondrial functioning in ME/CFS."

Chronic Fatigue Syndrome activist's 2018 research summary leaves out HHV-6 and the work of Bhupesh Prusty

The Chronic Fatigue Syndrome and HHV-6 Scientist of the Year 

Meet the scientist who may prove that HHV-6 is the Chronic Fatigue Syndrome virus

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

Breaking news about Dr. Prusty's game-changing HHV-6 & Chronic Fatigue Syndrome research from the University of Wurzburg 

The major Chronic Fatigue Syndrome organization is supporting the scientist who may show HHV-6 is the cause of Chronic Fatigue Syndrome. 

The Prusty study of HHV-6 in Chronic Fatigue Syndrome that Solve ME/CFS supported.

Does the research of Bhupesh Prusty support the theory that HHV-6 is causing oxidative stress in AIDS & CFS?

If Bhupesh Prusty wins a Nobel Prize for proving HHV-6 is the cause of Chronic Fatigue Syndrome, will he share it with Gallo or Beldekas?

Chronic Fatigue Syndrome patients are finally discovering Prusty's CFS and HHV-6 research  

Is HHV-6 altering the mitochondria in NK lymphocytes of Chronic Fatigue Syndrome patients?

Mitochondrial alterations in NK lymphocytes from ME/CFS patients

"Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disease characterized by profound fatigue, flu-like symptoms, trouble concentrating, and autonomic problems, all of which worsen after exertion. ME/CFS patients have impaired natural killer (NK) cell activity. NK lymphocytes are a critical first defense against viruses and cancer. ME/CFS patients have difficulties controlling viral infections and many develop non-Hodgkin’s lymphoma. Mitochondrial metabolism is crucial for immune cell function. Mitochondria dysfunction has been previously reported in ME/CFS, but it is not known whether the NK cells of these patients have altered mitochondrial metabolism that affect their activity and contribute to ME/CFS pathogenesis. More importantly, there is currently no efficient method to diagnose ME/CFS or assess efficacy of therapeutic interventions. The Bioenergetic Health Index (BHI) has been developed as promising and reliable surrogate readout of human health by measuring the bioenergetic status of immune cells. Variations in bioenergetic function in patient’s immune cells can reflect both metabolic stress and the mutable role of these cells in ME/CFS immunity and pathogenesis. In our study, we observed that the two main energy-generating mitochondrial pathways, oxidative phosphorylation and glycolysis (bioenergetics parameters), are deregulated in ME/CFS NK cells and in PBMCs. Moreover, we observed alterations in the morphology and membrane potential of the mitochondria of NK cells. These mitochondrial features can affect NK cell function and contribute to the severity of disease. To date, this is the first metabolism assessment of NK cells in ME/CFS and as potential new diagnostic tool for the disease."

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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