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Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis.
Sfera, Adonis; Osorio, Carolina; Zapata Martín Del Campo, Carlos M; Pereida, Shaniah; Maurer, Steve; Maldonado, Jose Campo; Kozlakidis, Zisis.
  • Sfera A; Patton State Hospital, San Bernardino, CA, United States.
  • Osorio C; Loma Linda University, Loma Linda, CA, United States.
  • Zapata Martín Del Campo CM; Psychiatry Service, Outpatient Consultation Department, National Institute of Cardiology Ignacio Chavez, Mexico, Mexico.
  • Pereida S; Loma Linda University, Loma Linda, CA, United States.
  • Maurer S; Patton State Hospital, San Bernardino, CA, United States.
  • Maldonado JC; Department of Internal Medicine, The University of Texas Rio Grande Valley, Edinburg, TX, United States.
  • Kozlakidis Z; International Agency for Research on Cancer (IARC), Lyon, France.
Front Cell Neurosci ; 15: 673217, 2021.
Article in English | MEDLINE | ID: covidwho-1282396
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.
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Full text: Available Collection: International databases Database: MEDLINE Type of study: Etiology study Topics: Long Covid Language: English Journal: Front Cell Neurosci Year: 2021 Document Type: Article Affiliation country: Fncel.2021.673217

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Full text: Available Collection: International databases Database: MEDLINE Type of study: Etiology study Topics: Long Covid Language: English Journal: Front Cell Neurosci Year: 2021 Document Type: Article Affiliation country: Fncel.2021.673217