SARS-CoV-2 Drives Host Cells: Some Key Points

The article addresses some mechanisms of interaction between SARS-CoV-2 and host cells. These include modalities of intracellular viral replication, pathways of host protein ubiquitination, the integration with the host genome and the kind of induced host immunity. The infection mechanism of a SARS-CoV-2 does not differ from that of many viruses, with which it shares morphological and functional characteristics. Therefore, more than discover, occurs to understand and follow the ways run by the virus. To replicate SARS-CoV-2 inserts into the cell a series of unavoidable instructions, aimed at producing copies of the its RNA and proteins. The cell is instigated to commit suicide. Such a sequence occurs in a) non-decoherent mode and dimension, both in the biochemical pathway and in its timing, and requires b) cell permissiveness. For these reasons (a & b) the sequence can be slow or fast, in a variable condition, according to cell proteoma and HLA. Clinically, the severity of the disease and the host susceptibility depend upon them. In the host SARS-CoV-2 spreads both at a local level (mucosal surface or organ) or via the bloodstream, with subsequent dissemination through all organs and different cell involvement. SARS-CoV-2 spread mechanisms may limit exposure of extracellular virus to humoral or cellular host defense system. This enables a long persistence of the SARS-CoV-2 in the host, with minimal or no clinical evidence, not differently from other viruses and can explain many peculiarities and difficulties in testing and predicting immunity against the virus. Moreover, virus serologic variants (and genome mutilation) evolve, with minimal cross-reactivity among them, but with a wide pattern of immune reactions in the host. Camouflage and latency spread mechanisms in SARS-Cov2 require further investigation. A full understanding of the phenomena described clarifies some of the singular characteristics of infection and pathogenesis of the COVID-19 disease.