tetano
Editor, Senior Moderator
Proc Natl Acad Sci U S A
. 2021 Aug 24;118(34):e2024358118.
doi: 10.1073/pnas.2024358118.
Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome
Bindu D Paul[SUP] 1 2 3 [/SUP], Marian D Lemle[SUP] 4 [/SUP], Anthony L Komaroff[SUP] 5 [/SUP], Solomon H Snyder[SUP] 1 2 3 [/SUP]
Affiliations
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.
Keywords: COVID-19; chronic fatigue syndrome; mitochondria; myalgic encephalomyelitis; redox.
. 2021 Aug 24;118(34):e2024358118.
doi: 10.1073/pnas.2024358118.
Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome
Bindu D Paul[SUP] 1 2 3 [/SUP], Marian D Lemle[SUP] 4 [/SUP], Anthony L Komaroff[SUP] 5 [/SUP], Solomon H Snyder[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 34400495
- DOI: 10.1073/pnas.2024358118
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.
Keywords: COVID-19; chronic fatigue syndrome; mitochondria; myalgic encephalomyelitis; redox.