Editorial: Infectious and inflammatory mechanistic underpinnings of CFS/ME (2023) Burton

Milo

Senior Member (Voting Rights)
There is no abstract but it is open access and quick read. Here is an excerpt:

Recent reanalysis of the DIOS (Dubbo study) cohort data focusing on genetic changes—including some associated with autoimmunity such as the inflammasome, IL6, IL1beta, IL10, and others—reaffirmed these earlier findings and findings are presented in this special edition of Frontiers in Neurology in “Predictors of chronic fatigue syndrome and mood disturbance after acute infection.” To put it simply: the severity of the initial insult or shock to the body's homeostasis is the best predictor of whether an individual goes on to develop CFS/ME. In the mini-review “Animal models for neuroinflammation and potential treatment methods,” Tamura et al., states the onset of CFS/ME in animals is often associated with neuroinflammation which follows either bacterial or viral infections and it is the degree of neuroinflammation that correlates with the severity of several CFS/ME symptoms

(Bolding is me adding explanation for the abbreviation)
 
A R Burton (of Sydney ) has previously published with A Lloyd which presumably explains the use of CFS/ME.

Fukuda is on the panel of editors for this research topic
 
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