P58(IPK): a novel "CIHD" member of the host innate defense response against pathogenic virus infection.

ABSTRACT: To support their replication, viruses take advantage of numerous cellular factors and processes. Recent large-scale screens have identified hundreds of such factors, yet little is known about how viruses exploit any of these. Influenza virus infection post-translationally activates P58(IPK), a cellular inhibitor of the interferon-induced, dsRNA-activated eIF2alpha kinase, PKR. Here, we report that infection of P58(IPK) knockout mice with influenza virus resulted in increased lung pathology, immune cell apoptosis, PKR activation, and mortality. Analysis of lung transcriptional profiles, including those induced by the reconstructed 1918 pandemic virus, revealed increased expression of genes associated with the cell death, immune, and inflammatory responses. These experiments represent the fi

SUBMITTER: Goodman AG 

PROVIDER: S-EPMC2677460 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature