Theiler's virus leader protein inhibits stress granule assembly through pkr inhibition

This work describes a new activity of the L protein of Theiler’s Murine Encephalomyelitis Virus (TMEV); the inhibition of stress granule assembly. Stress granules (SG) assemble in cells exposed to environmental stresses, such as viral infections. Because they trap essential translation factors, SG might constitute an obstacle to viral translation. Recent reports also suggest that they could be a platform where crosstalk between stress sensing and innate immunity signaling occur. We showed that TMEV infection is really prone to induce SG formation, but only when the L protein is defective, thereby uncovering a new inhibitory activity of L on SG formation. We further demonstrated that L blocks SG formation by preventing the interaction between viral double-stranded RNA and the cellular protein PKR, a kinase whose activation triggers SG assembly.