Canine parvovirus NS1 induces host translation shutoff by reducing mTOR phosphorylation

• DOI: 10.1128/jvi.01463-24
• Publication Date: 2024-11-27T14:06:59Z
• Authors: Xinrui Wang; Xiangqi Hao; Yaning Zhao; Xiangyu Xiao; Shoujun Li; Pei Zhou
• Keywords: Canine parvovirus

Canine parvovirus type 2 (CPV-2) is a member of the Parvoviridae family, characterized by its small, non-enveloped virions containing linear single-stranded DNA genome approximately 5 kb. Parvoviruses entirely reliant on host cell's division machinery for replication. In this study, we demonstrate that CPV-2 infection triggers translation shutoff, process in which nonstructural protein 1 (NS1) plays pivotal role. Our findings indicate NS1-induced shutoff not associated with transcription, degradation pathways, or eIFα phosphorylation, but rather involves reduction phosphorylation mammalian target rapamycin (mTOR). conclusion, research reveals NS1 induces reducing mTOR mechanism could potentially inform development more efficacious control and therapeutic strategies other parvoviral infections. Autonomous parvoviruses, possess compact genomes, are obligate intracellular parasites necessitate cell their replication cycle. Consequently, modulation usurpation cellular hypothesized to facilitate immune evasion, enhance viral transmission, perpetuate long-term infection. Despite biological significance, precise mechanisms autonomous parvoviruses regulate remain understudied. study elucidates through attenuation phosphorylation. This may enable virus subvert response engender pathogenic effects.