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10.3389/fmed.2020.564170

http://scihub22266oqcxt.onion/10.3389/fmed.2020.564170
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33043037!7517715!33043037
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suck abstract from ncbi


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pmid33043037      Front+Med+(Lausanne) 2020 ; 7 (ä): 564170
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  • Moderate Fever Cycles as a Potential Mechanism to Protect the Respiratory System in COVID-19 Patients #MMPMID33043037
  • Guihur A; Rebeaud ME; Fauvet B; Tiwari S; Weiss YG; Goloubinoff P
  • Front Med (Lausanne) 2020[]; 7 (ä): 564170 PMID33043037show ga
  • Mortality in COVID-19 patients predominantly results from an acute respiratory distress syndrome (ARDS), in which lungs alveolar cells undergo programmed cell death. Mortality in a sepsis-induced ARDS rat model is reduced by adenovirus over-expression of the HSP70 chaperone. A natural rise of body temperature during mild fever can naturally accumulate high cellular levels of HSP70 that can arrest apoptosis and protect alveolar lung cells from inflammatory damages. However, beyond 1-2 h of fever, no HSP70 is being further produced and a decreased in body temperature required to the restore cell's ability to produce more HSP70 in a subsequent fever cycle. We suggest that antipyretics may be beneficial in COVID-19 patients subsequent to several hours of mild (<38.8 degrees C) advantageous fever, allowing lung cells to accumulate protective HSP70 against damages from the inflammatory response to the virus SARS-CoV-2. With age, the ability to develop fever and accumulate HSP70 decreases. This could be ameliorated, when advisable to do so, by thermotherapies and/or physical training.
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