Department of Cell Biology, Harvard Medical School, Boston, MA 02115.
Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115.
Proc Natl Acad Sci U S A. 2022 Sep 20;119(38):e2209514119. doi: 10.1073/pnas.2209514119. Epub 2022 Sep 1.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cell entry starts with membrane attachment and ends with spike (S) protein-catalyzed membrane fusion depending on two cleavage steps, namely, one usually by furin in producing cells and the second by TMPRSS2 on target cells. Endosomal cathepsins can carry out both. Using real-time three-dimensional single-virion tracking, we show that fusion and genome penetration require virion exposure to an acidic milieu of pH 6.2 to 6.8, even when furin and TMPRSS2 cleavages have occurred. We detect the sequential steps of S1-fragment dissociation, fusion, and content release from the cell surface in TMPRRS2-overexpressing cells only when exposed to acidic pH. We define a key role of an acidic environment for successful infection, found in endosomal compartments and at the surface of TMPRSS2-expressing cells in the acidic milieu of the nasal cavity.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的细胞进入始于膜附着,结束于刺突(S)蛋白催化的膜融合,这取决于两个切割步骤,即在产生细胞中通常由弗林蛋白酶进行,在靶细胞中由 TMPRSS2 进行。内体组织蛋白酶可以同时进行这两种切割。通过实时三维单病毒跟踪,我们表明融合和基因组渗透需要病毒暴露在 pH6.2 到 6.8 的酸性环境中,即使弗林蛋白酶和 TMPRSS2 的切割已经发生。只有在暴露于酸性 pH 值时,我们才能在过表达 TMPRSS2 的细胞中检测到 S1 片段解离、融合和内容物从细胞表面释放的连续步骤。我们定义了成功感染的酸性环境的关键作用,该作用存在于内体区室中和鼻腔酸性环境中表达 TMPRSS2 的细胞表面。