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

The third recent new outbreak causing large-scale pandemics through the world and provoked by a new coronavirus, named SARS-CoV-2, exhibits terrifying spread out of control and qualifies for one of the largest scale pandemic since one century. More frightening, many people that are infected don't present clinical signs, which helps its spread, making it likely endemic for a long time. A minority of people (about 15% of infected) endures degraded conditions requiring intensive care unit for treatment. The virus presently spreads throughout the world and could end up with the death rate of 2-3% of infected population. Metagenomic RNA sequencing along with the phylogenetic analysis of the complete viral genome from a sample of broncho-alveolar lavage fluid of a patient infected by so called 'Wuham coronavirus' (now referred to as SARS-CoV -2) have been performed [1, 2 ] . These analyses have shown that this strain is very close to a group of SARS like coronaviruses previously found in bats in China [1, 2] . The high homology of the predicted protein of the RBD domain of the spike protein with the precedent SARS-CoV hints that the human angiotensin-converting enzyme 2 (ACE2) acts as a receptor for fixation and entry to human host cells [3, 4] . The cell entry is a multi-step process ordered cascade of events that involves viral attachment to the cell surface, receptor binding, protease processing and endocytose.