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Zhong Nan Da Xue Xue Bao Yi Xue Ban · May 2020
ReviewPotential pathogenesis of severe acute respiratory syndrome coronavirus 2.
- Tong Wu, Hanqi Zhang, Erya Hu, and Jian Ma.
- Cancer Research Institute, School of Basic Medical Science, Central South University; NHC Key Laboratory of Carcinogenesis (Central South University); Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education (Central South University), Changsha 410078, China. xiaojuzizwz@163.com.
- Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2020 May 28; 45 (5): 591-597.
AbstractThe 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.
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