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  Indian J Med Microbiol
 

Figure 1: Mitochondria and anti-viral SARS-CoV-2 response. The entry of the SARS-CoV-2 into the target cell such as type II alveolar epithelial cells is facilitated by androgen induced serine protease, trans-membrane serine protease 2 (TMPRSS2). The presence of SARS-CoV-2 is sensed by retinoic-acidinducible gene-I (RIG-I) like receptors (RLRs), major sensors of viral RNA. The antiviral protein mitochondrial anti-viral signalling protein (MAVS) on the outer mitochondrial membrane (OMM) gets activated which then forms the NLRP3/MFN2/MAVS inflammasome complex to induce type 1-IFN anti-SARS-CoV-2 response. The mitochondria can ensue the shift of the respiratory dependency of the host cells from the tricyclic antidepressant (TCA) cycle to β-oxidation aiding in the macrophage or immune cell phenotype switch from pro-inflammatory (M1) to the anti-inflammatory (M2) phenotype, a possible anti-SARS-CoV-2 response adapted by robust mitochondria as seen in athletes and females as compared to males.

Figure 1: Mitochondria and anti-viral SARS-CoV-2 response. The entry of the SARS-CoV-2 into the target cell such as type II alveolar epithelial cells is facilitated by androgen induced serine protease, trans-membrane serine protease 2 (TMPRSS2). The presence of SARS-CoV-2 is sensed by retinoic-acidinducible gene-I (RIG-I) like receptors (RLRs), major sensors of viral RNA. The antiviral protein mitochondrial anti-viral signalling protein (MAVS) on the outer mitochondrial membrane (OMM) gets activated which then forms the NLRP3/MFN2/MAVS inflammasome complex to induce type 1-IFN anti-SARS-CoV-2 response. The mitochondria can ensue the shift of the respiratory dependency of the host cells from the tricyclic antidepressant (TCA) cycle to β-oxidation aiding in the macrophage or immune cell phenotype switch from pro-inflammatory (M1) to the anti-inflammatory (M2) phenotype, a possible anti-SARS-CoV-2 response adapted by robust mitochondria as seen in athletes and females as compared to males.