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Autopsy findings: Summary of discussions


almost there...
Laurentians, Quebec
I've always thought they should put more effort into studying our bodies post-mortem: look for pathogens, toxins, and changes in tissues. Nobody wants to have to do a brain biopsy on a living patient.

When you begin looking at brain slices and other tissue samples unimpeded you might just begin finding stuff that shouldn't be there. Perhaps I've grown cynical but I don't think they actually want to know what garbage is in us and keeping us ill. They'd rather blame it on genes, cute theories where bodies just get stuck in illness without a perpetuating pathogen, or just leave it as a mystery. I mean who doesn't like a good mystery?

SNT Gatchaman

Senior Member
New Zealand
May be off-topic as relates specifically to coronaviruses (esp SARS-CoV-2).

[Preprint] COVID-19 Neuropathology: evidence for SARS-CoV-2 invasion of Human Brainstem Nuclei

SARS-CoV-2 viral antigens, on the other hand, were confined to specific loci of the CNS [...] appears to be localized preferentially within neurons of the vagal nuclei of the medulla and the substantia nigra

ACE2 Receptor and TMPRSS-2 protein immunohistochemistry support this topographical localization, with neurons within the dorsal motor nucleus of the vagus, solitary tract nucleus, nucleus Ambiguus and Substantia Nigra being moderately immunoreactive

SARS-CoV and MERS-CoV, which are known to be able to infect the brainstem, and particularly the dorsal motor nucleus of the vagus, solitary tract nucleus and nucleus ambiguus.


Senior Member
The research about the virus being confined to specific areas of the brain supports my beliefs about finding the root cause of ME: that it may involve a slight alteration of a fairly small number of brain cells, which would be very difficult to find via imaging or autopsies (the alteration might not show up in non-living tissue). If that's true, we'd be better off trying to find factors that alter ME in individuals, and use that to identify the root cause or just find an effective treatment. My guess is that the factors have to be able to alter brain cells, so the ability to cross the BBB is critical. Okay, it could be metabolites that can cross the BBB, but then someone could figure out which metabolite.

This method doesn't require that the factors reduce ME symptoms. Ones that reliably worsen ME can also point to the root cause. If some chemical reliably made 80+% of PWME worse, they could search for counteragents, and ones that worked would help identify the root cause. The method is similar to how researchers genetically alter subjects to knock out a gene, which then reveals what that gene normally did.


Senior Member
Dr Prusty examines three brains of deceased ME patients.


Tissue specific signature of HHV-6 infection in ME/CFS
Francesca Kasimir1, Danny Toomey2, Zheng Liu1, Agnes Kaiping1, Maria Eugenia Ariza3 and Bhupesh K. Prusty1*
  • 1Julius Maximilian University of Würzburg, Germany
  • 2HHV-6 Foundation, United States
  • 3The Ohio State University, United States
Provisionally accepted:

The final, formatted version of the article will be published soon.
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First exposure to various human herpesviruses (HHVs) including HHV-6, HCMV and EBV does not cause a life-threatening disease. In fact, most individuals are frequently unaware of their first exposure to such pathogens. These herpesviruses acquire lifelong latency in the human body where they show minimal genomic activity required for their survival. We hypothesized that it is not the latency itself but a timely, regionally restricted viral reactivation in a sub-set of host cells that plays a key role in disease development. HHV-6 (HHV-6A and HHV-6B) and HHV-7 are unique HHVs that acquire latency by integration of the viral genome into sub-telomeric region of human chromosomes. HHV-6 reactivation has been linked to Alzheimer’s Disease, Chronic Fatigue Syndrome, and many other diseases. However, lack of viral activity in commonly tested biological materials including blood or serum strongly suggests tissue specific localization of active HHV-6 genome. Here in this paper, we attempted to analyze active HHV-6 transcripts in postmortem tissue biopsies from a small cohort of ME/CFS patients and matched controls by fluorescence in situ hybridization using a probe against HHV-6 microRNA (miRNA), miR-aU14. Our results show abundant viral miRNA in various regions of the human brain and associated neuronal tissues including the spinal cord that is only detected in ME/CFS patients and not in controls. Our findings provide evidence of tissue-specific active HHV-6 and EBV infection in ME/CFS, which along with recent work demonstrating a possible relationship between herpesvirus infection and ME/CFS, provide grounds for renewed discussion on the role of herpesviruses in ME/CFS.