SARS-CoV-2 might manipulate against its host the immunity RNAi/Dicer/Ago system Does mitochondria collapse upon COVID-19 infection?

Claude Pasquier; Alain Robichon

This effector response might have overwhelmed the initial RNAi role, which is inferred by the accumulation of virus-derived small RNAs (vsRNAs) in mammal host cells for which any specified functions have been found [7] . The question whether RNA virus infection of mammalian cells can trigger an effective and powerful antiviral RNAi weapon remains unknown and little documented as no siRNAs of viral origin were experimentally found in mammal infected cells in contrast with in plants and invertebrates [8] . The absence of virus specific siRNAs in mammal cells remains presently a puzzling observation for which an explanation could be the scarcity of intra RNA pairing offered by the virus genomes. In light of their evolutionary success to replicate in mammal host through genetic innovation, RNA viruses have developed mechanisms of avoidance of host immunity/defense by masking their own RNA sequences or sheltering away from the cytosol and/or receptor sensors in order to escape the battlefield leading to their own degradation.