Figure.

Cell entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occurs through the interaction of the receptor-binding domain of the spike protein with angiotensin-converting enzyme 2 (ACE2) receptor, which causes cleavage/activation of the spike protein by cellular proteases. After fusion of the viral envelope with the cellular membrane, the viral positive-strand RNA is translated into a polyprotein and cleaved by viral proteases, forming the replicase-transcriptase complex (RTC) within double-membrane vesicles. The RTC that contains error-prone RNA-dependent RNA polymerase then mediates viral RNA replication, which in turn leads to viral protein synthesis and to production of more viral RNA. Viral proteins translocate to the endoplasmic reticulum (ER), in which they assemble in the ER-Golgi intermediate compartment (ERGIC), and daughter virions are released by exocytosis. These daughter virions often contain mutations due to the error-prone nature of the replication cycle, and these mutants may alter different aspects of coronavirus disease 2019 pathophysiology, which can be good (green), bad (red), or indifferent (yellow) to the human host. E, envelope; M, membrane; N, nucleocaspsid; N/A, not applicable; S, spike; (+)gRNA, viral positive strand genomic RNA; (−)gRNA, viral negative strand genomic RNA; (+)sgRNA, positive strand (+) subgenomic RNA; (−)sgRNA, negative strand subgenomic RNA.