The EMCV protein 2B* is required for efficient cell lysis via both caspase-3-dependent and -independent pathways during infection.

ABSTRACT: 2B* is a poorly characterized protein encoded by an overlapping ORF in the genome of encephalomyocarditis virus (EMCV). We have previously found 2B* to have a role in innate immune antagonism; however, this role is distinct from an earlier described phenotype whereby 2B*KO viruses exhibit extremely small plaques compared to WT. Here, we report that the small plaque phenotype is recapitulated by novel EMCV mutant viruses harbouring mutations across the C-terminal domain of 2B*, confirming a functional role of 2B* in promoting viral spread. We found that 2B*KO EMCV displays impaired extracellular virus titres compared to WT EMCV, despite producing a similar number of infectious particles overall. This correlates with a reduction in cell lysis and lower levels of caspase-3 cleavage occurring

SUBMITTER: Nguyen SK 

PROVIDER: S-EPMC11811419 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature