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    ORF3a of SARS-CoV-2 promotes lysosomal exocytosis-mediated viral egress, Dev Cell, 11 Oct 2021

    發布時間:2021年10月11日

    Developmental Cell, 11 October, 2021, DOI:https://doi.org/10.1016/j.devcel.2021.10.006

    ORF3a of SARS-CoV-2 promotes lysosomal exocytosis-mediated viral egress

    Di Chen, Qiaoxia Zheng, Long Sun, Yan Li, Hongyu Deng, Hong Zhang

    Abstract

    Viral entry and egress are important determinants of virus infectivity and pathogenicity. β-Coronaviruses, including the COVID-19 virus SARS-CoV-2 and MHV, exploit the lysosomal exocytosis pathway for egress. Here we show that SARS-CoV-2 ORF3a, but not SARS-CoV ORF3a, promotes lysosomal exocytosis. SARS-CoV-2 ORF3a facilitates lysosomal targeting of the BORC-ARL8b complex, which mediates trafficking of lysosomes to the vicinity of the plasma membrane, and exocytosis-related SNARE proteins. The Ca2+ channel TRPML3 is required for SARS-CoV-2 ORF3a-mediatd lysosomal exocytosis. Expression of SARS-CoV-2 ORF3a greatly elevates extracellular viral release in cells infected with the coronavirus MHV-A59 which itself lacks ORF3a. In SARS-CoV-2 ORF3a, Ser171 and Trp193 are critical for promoting lysosomal exocytosis and blocking autophagy. When these residues are introduced into SARS-CoV ORF3a, it acquires the ability to promote lysosomal exocytosis and inhibit autophagy. Our results reveal a mechanism by which SARS-CoV-2 interacts with host factors to promote its extracellular egress.

    文章鏈接:https://www.cell.com/developmental-cell/fulltext/S1534-5807(21)00807-8

     

     

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