Functional impairment of eIF4A and eIF4G factors correlates with inhibition of influenza virus mRNA translation.

Influenza virus mRNAs contain a 5'-cap structure followed by short cell-derived heterogeneous oligonucleotides and they are polyadenylated. However, selective translation of viral mRNAs occurs upon infection. Thus, we have studied whether differential requirements for the eIF4F components on viral and cellular translation could mediate this selectivity. We have previously reported that influenza virus infection proceeds efficiently upon functional impairment of the cap-binding factor eIF4E. Now, the requirements for the eIF4A helicase and the eIF4G scaffolding factor have been examined. The two proteins are essential for viral translation both in in vivo and in vitro analysis. Consequently, viral mRNAs do not contain cis-acting signals that could mediate eIF4A and eIF4G independence and trans-acting viral proteins do not replace their function. Thus, eIF4A and eIF4G proteins are not responsible for the selective translation of viral mRNAs and the translational shut-off of cellular protein synthesis observed in influenza virus infected cells.