Fig. 1.

a Domain arrangement of SARS-CoV-2 spike protein. SS signal sequence, NTD N-terminal transactivation domain, RBD receptor binding domain, SD subdomain, FP fusion peptides, HR1 heptad repeat 1, HR2 heptad repeat 2, CD connector domain, S1/S2 and S2′ protease cleavage sites, TM transmembrane domain, CT cytoplasmic tail. b Host cell entry and replication of SARS-CoV-2. SARS-CoV-2 infection starts with the binding of spike protein with ACE2 receptor and the invasion process is triggered by host cell proteases (furin, trypsin, TMPRSS2 and cathepsin). SARS-CoV-2 releases RNA into the host cell, and the RNA is translated into viral replicase polyproteins pp1a and pp1ab, and subsequently cleaves into NSPs. The full-length negative strand RNA copies of the viral genome are produced by the enzyme replicase using the full-length positive-strand RNA genome as a template. During transcription, RNA polymerase produces a series of subgenomic mRNAs and translates into viral proteins [S (Spike), E (Envelope), N (Nucleocapsid), and M (Membrane)]. The viral proteins and the genome RNA are assembled into virions in Golgi and ER (endoplasmic reticulum), which are budding into ERGIC (ER–Golgi intermediate compartment) and released out of the cell via vesicles