Respiratory Syncytial Virus (RSV) optimizes the translational landscape during infection.

Viruses strongly rely on the host's translational machinery to produce viral proteins required for replication. However, it is unknown how viruses that do not globally inhibit cap-dependent translation compete with abundant host transcripts for ribosomes. In this study, we found that respiratory syncytial virus (RSV) infection results in redistribution of 80S monosomes into the polysomes. High-throughput sequencing of translating transcripts revealed that low translation efficiency transcripts become more efficient at ribosome recruitment which are virus-resembling AU-rich host transcripts. Finally, we also uncover that AU-rich RNA binding protein RSV-M2-1 interacts with polysomes through contacts to mRNA. These findings revealed that RSV optimizes the translational landscape rather than inhibiting host translation.