Abstract
The aim of this scoping review was to identify knowledge gaps and to describe the current state of the research on the association between TMPRSS2 and the essential beta coronaviruses (Beta-CoVs) infection and the molecular mechanisms for this association. We searched MEDLINE (OVID), EMBASE, and the Cochrane Central Register of Controlled Trials (CENTRAL). We included 13 studies. Evidence shows an essential role of TMPRSS2 in Spike protein activation, entry, and spread into host cells. Co-expression of TMPRSS2 with cell surface receptors (ACE2 or DPP4) increased virus entry. This serine protease is involved in the formation of large syncytia between infected cells. TMPRSS2 cleaved the Spike protein of SARS-CoV, SARS-CoV-2, and MERS-CoV, and increased virus propagation. Accumulating evidence suggests that TMPRSS2 is an essential protease for virus replication. We highlighted its critical molecular role in membrane fusion and the impact in viral mRNA replication, then promoting/driving pathogenesis and resistance.
Keywords: Betacoronavirus; Gene; MERS-CoV; SARS-CoV; SARS-CoV-2; TMPRSS2.
【저자키워드】 SARS-CoV-2, SARS-CoV, MERS-CoV, Betacoronavirus, TMPRSS2., Gene, 【초록키워드】 ACE2, TMPRSS2, Pathogenesis, spike, knowledge, Infection, protease, MERS, molecular mechanism, Betacoronavirus, Spike protein, DPP4, Replication, Spread, Protein, controlled trials, mRNA, Syncytia, Research, virus entry, virus replication, membrane fusion, molecular, Critical, association, Evidence, host cells, cell surface receptor, cell surface receptors, Activation, Serine, infected cells, molecular mechanisms, serine protease, CENTRAL, OVID, beta-CoVs, virus propagation, identify, involved, searched, in viral, Controlled, cleaved, the Spike, beta coronavirus, 【제목키워드】 mechanism, association, beta coronavirus,