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P58IPK, a potential virulence factor that regulates influenza viral protein synthesis

, : P58IPK, a potential virulence factor that regulates influenza viral protein synthesis. Biophysical Journal 86(1): 89a, January

If without proper viral countermeasures, influenza virus infection may cause the inhibition of viral and host cell protein synthesis through the phosphorylation of eIF2alpha via PKR, a dsRNA-activated eIF2alpha kinase. Not surprisingly, influenza virus has developed mechanisms to avoid this protein synthesis shutdown. Influenza virus recruits a cellular protein, P58IPK, to down-regulate PKR, thus relieving the block in viral protein synthesis. P58IPK also down-regulates PERK, an endoplasmic reticulum (ER)-localized eIF2alpha kinase that is induced during ER stress and which is important for proper glucose metabolism. It is likely, therefore, that influenza infection also causes ER stress, which leads to the activation of P58IPK, thus allowing the translation of viral proteins. These observations demonstrate that P58IPK is responsive to multiple signals and provides a mechanism for modulating translational activity during influenza infection. To further characterize the role of P58IPK, we generated P58IPK knockout (KO) mice. These mice display a diabetic phenotype, possibly due to a defect in PERK regulation. Mouse embryonic fibroblasts (MEFs) from both KO and wild-type (WT) mice were isolated to monitor the phosphorylation state of eIF2alpha and rates of viral protein synthesis during influenza infection. Consistent with our hypothesis, virus-infected MEFs from p58IPK KO mice exhibited increased levels of phosphorylated eIF2alpha and lower levels of viral protein synthesis. These data indicate that influenza virus may replicate less efficiently in the absence of P58IPK, and that the lower level of viral protein synthesis may be due to a higher level of PKR and/or PERK activity. These results further suggest P58IPK is a virulence factor recruited by influenza, and its absence may lead to attenuation of virus replication. The study of the role of p58IPK may therefore offer insights about possible therapeutics for influenza.


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