Mammalian cells respond to various environmental stress, including virus infection, by arresting cytoplasmic mRNA, protein translation element and RNA binding proteins to form stress granules (SGs). In this study, we studied the mechanism involved in newcastle disease virus (NDV) induced SGs. Next we examined the specific components in NDV-induced SGs. Finally, we determined the role of SG in NDV infection and explored the concrete mechanism involved in how SG regulate virus replication. The main results of this study include:-NDV induced stable formation of SG in HeLa cells. NP protein was specifically recruited into SGs.-NDV infection reduced host protein translation over the time. Virus induced SG formation mainly through PKR/eIF2? pathway. NDV-induced SGs requires ongoing protein synthesis and contain the small ribosomal subunit and key components in eukaryotic translation initiation process-Microtubule disruption leads to the formation of small SGs post NDV infection-Depletion of endogenous TIA-1 and TIAR reduced NDV replication and increased global protein translation on HeLa cells-NDV-induced SGs contain predominantly cellular mRNA but not viral mRNA. |