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10.1016/j.isci.2020.101631

http://scihub22266oqcxt.onion/10.1016/j.isci.2020.101631
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33015593!7524535!33015593
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suck abstract from ncbi


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pmid33015593      iScience 2020 ; 23 (10): 101631
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  • Mitochondria: In the Cross Fire of SARS-CoV-2 and Immunity #MMPMID33015593
  • Burtscher J; Cappellano G; Omori A; Koshiba T; Millet GP
  • iScience 2020[Oct]; 23 (10): 101631 PMID33015593show ga
  • The pathophysiology, immune reaction, and differential vulnerability of different population groups and viral host immune system evasion strategies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are not yet well understood. Here, we reviewed the multitude of known strategies of coronaviruses and other viruses to usurp mitochondria-associated mechanisms involved in the host innate immune response and put them in context with the current knowledge on SARS-CoV-2. We argue that maintenance of mitochondrial integrity is essential for adequate innate immune system responses and to blunt mitochondrial modulation by SARS-CoV-2. Mitochondrial health thus may determine differential vulnerabilities to SARS-CoV-2 infection rendering markers of mitochondrial functions promising potential biomarkers for SARS-CoV-2 infection risk and severity of outcome. Current knowledge gaps on our understanding of mitochondrial involvement in SARS-CoV-2 infection, lifestyle, and pharmacological strategies to improve mitochondrial integrity and potential reciprocal interactions with chronic and age-related diseases, e.g., Parkinson disease, are pointed out.
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