"Severe acute respiratory syndrome coronavirus (SARS-CoV) is one of the most pathogenic human coronaviruses. Virulence is reflected in the molecular interplay between virus and host cells. Here we show a strategy of how SARS-CoV antagonizes the host antiviral factor p53, which impairs viral replication. The papain-like protease of the nonstructural protein 3 of SARS-CoV and other coronaviruses physically interact with and stabilize E3 ubiquitin ligase ring-finger and CHY zinc-finger domain-containing 1 (RCHY1), thereby augmenting RCHY1-mediated degradation of p53. The SARS-unique domain (SUD) enhances these effects. Knockout of p53 promotes replication of SARS-CoV replicons and of infectious virus. Taken together we identify cellular p53 as antiviral measure of coronavirus-infected cells, which is counteracted via the stabilization of RCHY1 by viral SUD and papain-like protease (PLpro) proteins and via ubiquitination of p53. "
https://www.pnas.org/content/113/35/E5192
The virus can infect the immune cells and cause lymphopenia. So in patients recently recovered from the disease, there is a gap that infections and cancers can occur easier.
https://www.nature.com/articles/s41577-020-00439-1#:~:text=Lymphopenia%20and%20systemic%20viral%20dissemination,SARS-CoV-2%20infection.
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