Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Bindu D. Paul, Marian D. Lemle, Anthony L. Komaroff, Solomon H. Snyder

Research output: Contribution to journalReview articlepeer-review

Abstract

Although most patients recover from acute COVID-19, some experience postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC). One subgroup of PASC is a syndrome called “long COVID-19,” reminiscent of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating condition, often triggered by viral and bacterial infections, leading to years-long debilitating symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, and orthostatic intolerance. Some are skeptical that either ME/CFS or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence that people with acute COVID-19 and with ME/CFS have biological abnormalities including redox imbalance, systemic inflammation and neuroinflammation, an impaired ability to generate adenosine triphosphate, and a general hypometabolic state. These phenomena have not yet been well studied in people with long COVID-19, and each of them has been reported in other diseases as well, particularly neurological diseases. We also examine the bidirectional relationship between redox imbalance, inflammation, energy metabolic deficits, and a hypometabolic state. We speculate as to what may be causing these abnormalities. Thus, understanding the molecular underpinnings of both PASC and ME/CFS may lead to the development of novel therapeutics.

Original languageEnglish (US)
Article numbere2024358118
JournalProceedings of the National Academy of Sciences of the United States of America
Volume118
Issue number34
DOIs
StatePublished - Aug 24 2021

Keywords

  • COVID-19
  • Chronic fatigue syndrome
  • Mitochondria
  • Myalgic encephalomyelitis
  • Redox

ASJC Scopus subject areas

  • General

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