Lipid rafts are involved in SARS-CoV entry into Vero E6 cells.
Lipid rafts are involved in SARS-CoV entry into Vero E6 cells.
复制标题
脂质筏参与SARS-COV进入Vero E6细胞。
DOI：
10.1016/j.bbrc.2008.02.023
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发表时间：
2008-05-02
影响因子：
3.1
通讯作者：
Tam JP
中科院分区：
文献类型：
--
作者：
Lu Y;Liu DX;Tam JP
脂筏通常作为某些病毒的进入位点。在此，我们报告 Vero E6 细胞中的脂筏参与了严重急性呼吸综合征冠状病毒（SARS-CoV）的进入。感染性测定表明，假型 SARS-CoV 的有效感染需要脂筏的完整性。用 MβCD 消耗质膜胆固醇，使筏驻留标记 Caveolin-1 和 SARS-CoV 受体 ACE2 重新定位到非筏环境，但没有显着改变 ACE2 的表面表达。 MβCD 治疗可将假型 SARS-CoV 的感染性抑制 90%。生化分级和共聚焦成像证实 ACE2 与筏驻留标记共定位。此外，SARS-CoV S蛋白（S1188HA）的胞外域在与其受体结合后可以与脂筏结合，并与脂筏驻留标记神经节苷脂GM1共定位。 S1188HA 的结合不受质膜胆固醇消耗的影响。综上所述，我们的结果支持脂筏是 SARS-CoV 的入口。
Lipid rafts often serve as an entry site for certain viruses. Here, we report that lipid rafts in Vero E6 cells are involved in the entry of severe acute respiratory syndrome coronavirus (SARS-CoV). Infectivity assay showed the integrity of lipid rafts was required for productive infection of pseudotyped SARS-CoV. Depletion of plasma membrane cholesterol with MβCD relocalized raft-resident marker caveolin-1 as well as SARS-CoV receptor ACE2 to a nonraft environment, but did not significantly change the surface expression of ACE2. MβCD-treatment inhibited infectivity of pseudotyped SARS-CoV by 90%. Biochemical fractionation and confocal imaging confirmed that ACE2 colocalized with raft-resident markers. Furthermore, an ectodomain of SARS-CoV S protein (S1188HA) could associate with lipid rafts after binding to its receptor, and colocalize with raft-resident marker ganglioside GM1. The binding of S1188HA was not affected by depleting plasma membrane cholesterol. Taken together, our results support that lipid rafts serve as an entry port for SARS-CoV.
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