The SHFV nsp2 and nucleocapsid proteins recruit G3BP1 to sites of viral replication, but stress granules are not induced by the infection.

ABSTRACT: Stress granules (SGs) are dynamic, cytoplasmic foci that form in response to environmental stresses, including viral infections, and function to restore cellular homeostasis by regulating mRNA translation, storage, and decay. To inhibit SG formation and subvert their antiviral effects, viruses from diverse families sequester or cleave G3BP1, the key SG nucleating protein. We found that an infection with simian hemorrhagic fever virus (SHFV), a member of the family Arteriviridae, does not induce the formation of bona fide SGs despite inducing phosphorylation of PKR and eIF2α. The SG proteins, G3BP1, G3BP2, TIA-1, Caprin-1, and USP10, but not the translation initiation proteins, eIF3A, eIF4G, and small ribosomal protein S6 (rpS6), were redistributed into foci located in the sam

SUBMITTER: Lavender AA 

PROVIDER: S-EPMC12282152 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature