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10.1016/j.csbj.2021.04.001

http://scihub22266oqcxt.onion/10.1016/j.csbj.2021.04.001
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33850607!8028701!33850607
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suck abstract from ncbi


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pmid33850607      Comput+Struct+Biotechnol+J 2021 ; 19 (ä): 1933-1943
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  • Dependence of SARS-CoV-2 infection on cholesterol-rich lipid raft and endosomal acidification #MMPMID33850607
  • Li X; Zhu W; Fan M; Zhang J; Peng Y; Huang F; Wang N; He L; Zhang L; Holmdahl R; Meng L; Lu S
  • Comput Struct Biotechnol J 2021[]; 19 (ä): 1933-1943 PMID33850607show ga
  • Coronavirus disease 2019 is a kind of viral pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the mechanism whereby SARS-CoV-2 invades host cells remains poorly understood. Here we used SARS-CoV-2 pseudoviruses to infect human angiotensin-converting enzyme 2 (ACE2) expressing HEK293T cells and evaluated virus infection. We confirmed that SARS-CoV-2 entry was dependent on ACE2 and sensitive to pH of endosome/lysosome in HEK293T cells. The infection of SARS-CoV-2 pseudoviruses is independent of dynamin, clathrin, caveolin and endophilin A2, as well as macropinocytosis. Instead, we found that the infection of SARS-CoV-2 pseudoviruses was cholesterol-rich lipid raft dependent. Cholesterol depletion of cell membranes with methyl-beta-cyclodextrin resulted in reduction of pseudovirus infection. The infection of SARS-CoV-2 pseudoviruses resumed with cholesterol supplementation. Together, cholesterol-rich lipid rafts, and endosomal acidification, are key steps of SARS-CoV-2 required for infection of host cells. Therefore, our finding expands the understanding of SARS-CoV-2 entry mechanism and provides a new anti-SARS-CoV-2 strategy.
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