严éæ¥æ§å¼å¸ç»¼åå¾å ç¶çæ¯2çæ½å¨è´çæºå¶./ 严éæ¥æ§å¼å¸ç»¼åå¾å ç¶çæ¯2çæ½å¨è´çæºå¶./ Potential pathogenesis of severe acute respiratory syndrome coronavirus 2.

The emergence of novel coronavirus pneumonia which was named as coronavirus disease 2019 (COVID-19) by the World Health Organization, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has posed a serious threat to public health. Notably, COVID-19 has rapidly spread around the world and large amount of people have been infected. There is imminent need to investigate the pathogenesis of SARS-CoV-2 and develop effective therapeutic strategies to contain the epidemic. The spike (S) protein of SARS-CoV-2 mediates viral entry into target cells, with S1 subunit binding to a cellular receptor and S2 subunit fusing viral and host membranes. Angiotensin-converting enzyme 2 (ACE2), previously known as a cell receptor of severe acute respiratory syndrome coronavirus (SARS-CoV), is putatively responsible for mediating COVID-19. In this review, we detail our current understanding of the interaction between S protein and ACE2 in the process of virus infection and the potential pathogenesis of SARS-CoV-2, which has critical implications for exploring the potential therapeutic strategies for COVID-19.