Review
Version 1
Preserved in Portico This version is not peer-reviewed
Post-Acute Sequelae And Mitochondrial Aberration In SARS-CoV-2 Infection
Version 1
: Received: 12 June 2024 / Approved: 18 June 2024 / Online: 18 June 2024 (15:41:08 CEST)
How to cite: Ward, C.; Schlichtholz, B. Post-Acute Sequelae And Mitochondrial Aberration In SARS-CoV-2 Infection. Preprints 2024, 2024061289. https://doi.org/10.20944/preprints202406.1289.v1 Ward, C.; Schlichtholz, B. Post-Acute Sequelae And Mitochondrial Aberration In SARS-CoV-2 Infection. Preprints 2024, 2024061289. https://doi.org/10.20944/preprints202406.1289.v1
Abstract
This review investigates links between post-acute sequelae of SARS-CoV-2 infection (PASC), post-infection viral persistence, mitochondrial involvement and aberrant innate immune response and cellular metabolism during SARS-CoV-2 infection. Advancement of proteomic and metabolomic studies now allows deeper investigation of alterations to cellular metabolism, autophagic processes and mitochondrial dysfunction caused by SARS-CoV-2 infection while computational biology and machine learning have advanced methodologies of predicting virus-host gene and protein interactions. Particular focus is given to interaction between viral genes and proteins with mitochondrial function and that of the innate immune system. Finally, the authors hypothesise that viral persistence may be a function of mitochondrial involvement in sequestration of viral genetic material. While further work is necessary to understand the mechanisms definitively, a number of studies now point to resolution of questions regarding the pathogenesis of PASC.
Keywords
SARS-CoV-2; PASC; long-Covid; mitochondria; mtDNA, autophagy; mitophagy; innate immunity; cell metabolism; reactive oxygen species
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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