Syntaxin-6 restricts SARS-CoV-2 infection by facilitating virus trafficking to autophagosomes.

ABSTRACT: Despite the diminishing global impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus continues to circulate and undergo mutations, posing ongoing challenges for public health. A comprehensive understanding of virus entry mechanisms is crucial for managing new epidemic strains. However, the cellular processes post-endocytosis remain largely unexplored. This study employs proximity labeling to examine proteins near ACE2 post-viral infection and identified syntaxin-6 (STX6) as a factor that inhibits SARS-CoV-2 infection by impeding the endocytic release of the virus. SARS-CoV-2 infection enhances early endosome recruitment of STX6. STX6 appears to hinder the maturation of viral particles-laden early endosomes into late endosomes, from which the virus could escape.

SUBMITTER: Sun H 

PROVIDER: S-EPMC12090716 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature