School of Medicine Publications and Presentations
Document Type
Article
Publication Date
6-25-2021
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.
Recommended Citation
Sfera A, Osorio C, Zapata Martín del Campo CM, Pereida S, Maurer S, Maldonado JC and Kozlakidis Z (2021) Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis. Front. Cell. Neurosci. 15:673217. doi: 10.3389/fncel.2021.673217
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Publication Title
Frontiers in Cellular Neuroscience
DOI
10.3389/fncel.2021.673217
Academic Level
faculty
Mentor/PI Department
Internal Medicine
Comments
Copyright 2021 Sfera, Osorio, Zapata Martín del Campo, Pereida, Maurer, Maldonado and Kozlakidis.