A Herpesvirus for Fibromyalgia?

SWAlexander

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Active Herpes Simplex Virus Found in FM Patients’ Guts

A New Virus for Fibromyalgia (and ME/CFS?)
Despite Pridgen’s success at getting a large trial together, we’ve been missing a significant piece of data – evidence that the herpes simplex viruses he’s stated that he believes are causing FM (and ME/CFS as well) are actually present. A recent study, “Gastric herpes simplex virus type 1 infection is associated with functional gastrointestinal disorders in the presence and absence of comorbid fibromyalgia: a pilot case–control study“, published in the Infection journal, reports they are – and not just in fibromyalgia.

The study, led by University of Alabama virologist Carole Duffy, examined gastric biopsies from 30 people who met the criteria for having both a functional gastrointestinal disorder (FGID) and fibromyalgia, 15 people with an FGID but not with FM, and 15 control patients who had undergone an endoscopy for something other than a functional gut issues (GI bleed, anemia, hiatal hernia, cancer, etc.).

Continue: https://www.healthrising.org/blog/2022/05/04/fibromyalgia-herpes-simplex-virus-gut/
 

GreenEdge

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HSV-1 is usually associated with oral herpes, but it can also spread to the genitals through oral sex. Most people know not to kiss or share a drink while a cold sore is present. The same goes for not performing oral sex while a cold sore is present.
  • HSV-1 is mainly transmitted by oral-to-oral contact, causing oral herpes (including symptoms known as cold sores), but it can also lead to genital herpes.
  • HSV-2 is a sexually transmitted infection that causes genital herpes.
 

SWAlexander

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News about Herpesviruses and interferons.

Selective inhibition of miRNA processing by a herpesvirus-encoded miRNA
Herpesviruses have mastered host cell modulation and immune evasion to augment productive infection, life-long latency and reactivation1,2. A long appreciated, yet undefined relationship exists between the lytic–latent switch and viral non-coding RNAs3,4. Here we identify viral microRNA (miRNA)-mediated inhibition of host miRNA processing as a cellular mechanism that human herpesvirus 6A (HHV-6A) exploits to disrupt mitochondrial architecture, evade intrinsic host defences and drive the switch from latent to lytic virus infection. We demonstrate that virus-encoded miR-aU14 selectively inhibits the processing of multiple miR-30 family members by direct interaction with the respective primary (pri)-miRNA hairpin loops. Subsequent loss of miR-30 and activation of the miR-30–p53–DRP1 axis triggers a profound disruption of mitochondrial architecture. This impairs induction of type I interferons and is necessary for both productive infection and virus reactivation. Ectopic expression of miR-aU14 triggered virus reactivation from latency, identifying viral miR-aU14 as a readily druggable master regulator of the herpesvirus lytic–latent switch. Our results show that miRNA-mediated inhibition of miRNA processing represents a generalized cellular mechanism that can be exploited to selectively target individual members of miRNA families. We anticipate that targeting miR-aU14 will provide new therapeutic options for preventing herpesvirus reactivations in HHV-6-associated disorders.
https://www.nature.com/articles/s41586-022-04667-4

In addition (transl): https://www.aerzteblatt.de/nachrich...rwachen?utm_source=dlvr.it&utm_medium=twitter

The Würzburg research group was also able to show that the viral micro-RNA is not only essential for virus replication, but also directly triggers the reactivation of the virus from the dormant state.

The research team now wants to understand the exact mechanism by which the viral microRNA triggers the reactivation of the virus.

Several groups from the Julius-Maximilians-Universität Würzburg are conducting interdisciplinary research on this topic. They come from the Institute for Virology and Immunobiology, from the Biozentrum chairs for Biochemistry, for Biotechnology and Biophysics as well as for Microbiology and from the Rudolf Virchow Center and the Helmholtz Institute for RNA-based Infection Research. Researchers from the Free University of Berlin and the University of Regensburg were also involved.
 
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