Infl uenza virus mRNAs are structurally indistinguishable from cellular ones as they bear 5'-cap structures and are polyadenylated at their 3'-ends. However, selective translation of viral mRNA, despite inhibition of host cell protein synthesis, occurs upon infection. Initiation of translation is a major target for gene expression regulation and viruses have evolved numerous unconventional mechanisms to recruit the cellular translational machinery. Often, the interactions of viral proteins with components of the eIF4F complex and with the viral mRNA allow selective translation of viral proteins interfering host cell protein synthesis.
In the presented work, we have evaluated the dependence on eIF4F components for infl uenza virus translation. Despite that infection proceeds effi ciently upon impairment of the eIF4E function, in vitro translation of isolated viral mRNA is strictly dependent on this factor, indicating that the in vivo independence is not the consequence of structural cis elements in the viral mRNA. However, viral translation seems to be strictly dependent on eIF4A and eIF4G activities both in in vitro and in vivo studies.
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