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COVID-19, which is caused by SARS-CoV-2, has been declared a global pandemic. Although effective strategies have been applied to treat the disease, much is still unknown about this novel virus. SARS-CoV-2 enters host cells through ACE2, which is a component of the angiotensin-regulating system. Binding of the SARS-CoV-2 S protein to ACE2 is a prerequisite for SARS-CoV-2 infection. Many studies have indicated a close relationship between ACE2 expression and SARS-CoV-2 infection. The structural basis of receptor recognition by SARS-CoV-2 has been analyzed in detail. The diversification of the ACE2 sequence due to ACE2 polymorphisms and alternative splicing has to a large extent affected the susceptibility of different species. Differential ACE2 expression makes specific populations more prone to be infected, and ACE2 also plays a role in the broad tropism of SARS-CoV-2 in human organs and tissues. In this review, we comprehensively summarize how the ACE2 expression profile affects the host range and tropism of SARS-CoV-2, which will provide mechanistic insights into the susceptibilities and outcomes of SARS-CoV-2 infection.
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10.1016/j.csbj.2020.11.032
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Comput_Struct_Biotechnol_J
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document_parses/pdf_json/888c8c7f4b1709e097e632774787fae14ca0e6bd.json
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document_parses/pmc_json/PMC7700767.xml.json
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ACE2 partially dictates the host range and tropism of SARS-CoV-2
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