Replication defective viral genomes exploit a cellular pro-survival mechanism to establish paramyxovirus persistence.

ABSTRACT: Replication defective viral genomes (DVGs) generated during virus replication are the primary triggers of antiviral immunity in many RNA virus infections. However, DVGs can also facilitate viral persistence. Why and how these two opposing functions of DVGs are achieved remain unknown. Here we report that during Sendai and respiratory syncytial virus infections DVGs selectively protect a subpopulation of cells from death, thereby promoting the establishment of persistent infections. We find that during Sendai virus infection this phenotype results from DVGs stimulating a mitochondrial antiviral-signaling (MAVS)-mediated TNF response that drives apoptosis of highly infected cells while extending the survival of cells enriched in DVGs. The pro-survival effect of TNF depends on the activity of

SUBMITTER: Xu J 

PROVIDER: S-EPMC5630589 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature