Figure 1. Life cycle of SARS‐CoV‐2 and antiviral drug targets.

Attachment of SARS‐CoV‐2 to its host cell is mediated by binding of the viral spike protein to the ACE2 receptor. After proteolytic cleavage of the S1 domain by the membrane‐anchored serine protease TMPRSS2, fusion of the viral and host cell membrane is initiated by the exposed S2 subunit. Alternatively, SARS‐CoV‐2 can invade the host cell upon endosomal uptake and activation of the spike protein by cathepsin L. Released viral RNA is translated by ribosomes of the host cell. Polyproteins pp1a/pp1ab are cleaved mainly by the viral main protease (3C‐like proteinase). Released non‐structural proteins form the replicase–transcriptase complex, which initiates the viral RNA synthesis machinery. Viral structure proteins and genomic RNA form new particles, which are released by exocytosis. The replication cycle of SARS‐CoV‐2 can be inhibited at various stadiums: viral entry (1‐2); protease inhibition (3), and RNA replication (4).