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HDL-scavenger receptor B type 1 facilitates SARS-CoV-2 entry #MMPMID33244168
Wei C; Wan L; Yan Q; Wang X; Zhang J; Yang X; Zhang Y; Fan C; Li D; Deng Y; Sun J; Gong J; Yang X; Wang Y; Wang X; Li J; Yang H; Li H; Zhang Z; Wang R; Du P; Zong Y; Yin F; Zhang W; Wang N; Peng Y; Lin H; Feng J; Qin C; Chen W; Gao Q; Zhang R; Cao Y; Zhong H
Nat Metab 2020[Dec]; 2 (12): 1391-1400 PMID33244168show ga
Responsible for the ongoing coronavirus disease 19 (COVID-19) pandemic, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects host cells through binding of the viral spike protein (SARS-2-S) to the cell-surface receptor angiotensin-converting enzyme 2 (ACE2). Here we show that the high-density lipoprotein (HDL) scavenger receptor B type 1 (SR-B1) facilitates ACE2-dependent entry of SARS-CoV-2. We find that the S1 subunit of SARS-2-S binds to cholesterol and possibly to HDL components to enhance viral uptake in vitro. SR-B1 expression facilitates SARS-CoV-2 entry into ACE2-expressing cells by augmenting virus attachment. Blockade of the cholesterol-binding site on SARS-2-S1 with a monoclonal antibody, or treatment of cultured cells with pharmacological SR-B1 antagonists, inhibits HDL-enhanced SARS-CoV-2 infection. We further show that SR-B1 is coexpressed with ACE2 in human pulmonary tissue and in several extrapulmonary tissues. Our findings reveal that SR-B1 acts as a host factor that promotes SARS-CoV-2 entry and may help explain viral tropism, identify a possible molecular connection between COVID-19 and lipoprotein metabolism, and highlight SR-B1 as a potential therapeutic target to interfere with SARS-CoV-2 infection.