COP I vesicles facilitate classical swine fever virus proliferation by transporting fatty acid synthase from the Golgi apparatus to the endoplasmic reticulum.

ABSTRACT: Classical swine fever virus (CSFV) is an enveloped, positive-sense, single-stranded RNA virus in the Flaviviridae family that remodels the cell's endomembrane for its own propagation. The early secretory pathway is exploited by viruses for their lifecycle, but the mechanism underlying this hijacking of the early secretory pathway in CSFV infection remains unknown. Here, we observed that disrupting the functions of the early secretory pathway organelles, the Golgi apparatus, the endoplasmic reticulum (ER), and coatomer protein I (COP I) vesicles and coatomer protein II (COP II) vesicles resulted in a significant inhibition of CSFV propagation. Further, we revealed that COP I vesicles were required for CSFV RNA replication, but not for the formation of viral replication complexes. The

SUBMITTER: Zhang L 

PROVIDER: S-EPMC12282108 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature