Fig. 1

Schematic representation of SARS-CoV-2 life cycle within host cells and potential antitumor drugs to treat COVID-19. The entry of SARS-CoV-2 into target cells requires fusion of viral and cellular membrane, which is initiated by conformational change of spike (S) protein. The S protein of SARS-CoV-2 binds to angiotensin- converting enzyme 2 (ACE2) on the host cells. If the host cell has low expression of type 2 transmembrane serine protease (TMPRSS2), the virus is internalized by endocytosis and transported to endolysosomes where S protein is processed by the protease cathepsin L (step 2) and then followed by membrane fusion (step 3). In the presence of TMPRSS2, it can directly induce the cleavage of S protein on the cell surface and trigger membrane fusion. Once SARS-CoV-2 enters into the cell, viral RNA is released into the cytoplasm (step 4) and is translated to two polyproteins, pp1a and pp1b (step 5), which are proteolytically cleaved into non-structural proteins (nsps) (step6). Then nsps form replicase-transcriptase complex (RTC) (step 7), which transcribes the viral genomic and subgenomic RNA (sgRNA) (steps 8 and 9). The sgRNAs are translated to produce structural and accessory proteins (step 10). Subsequently, nucleocapsids are assembled and bud into the lumen of the endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) (step 11) to produce a complete virus particle. Finally, virions traffic to the Golgi (step 12) and exit the host cell (step 13). Some antitumor drugs can target different stage of the viral cycle thus exerting antiviral effects. (Created with the assistance of smart.servier.com)