Key result
Influenza virus triggers cellular mRNA decay and protein shut-off independently of PKR and NS1 sequences.
Why the study?
The role of PKR activity and nuclear events in influenza virus-induced cellular protein synthesis shut-off was unclear.
Influenza virus-induced cell shut-off of protein synthesis is independent of PKR activity and NS1 C-terminal sequences.
Influenza-induced protein synthesis shutoff independent of PKR and NS1; leaves open alternative mechanisms and requires validation in human models.
The role of PKR activity in influenza virus-induced cell shut-off was studied by infection of PKR(+) or PKR(-) cell cultures and metabolic labeling in vivo. No differences in the synthesis of viral proteins or the decay of cellular protein synthesis were observed. To investigate the relevance of the inhibition of cellular pre-mRNA polyadenylation and nucleocytoplasmic transport in virus-induced shut-off, we carried out similar experiments with mutant viruses lacking C-terminal sequences of NS1 protein. No differences in the shut-off induced by mutant versus wild-type viruses were observed, indicating that these nuclear events are not relevant for shut-off. The analysis of cytoplasmic mRNA stability indicated that the accumulation of viral mRNA during the infection correlated with the progressive decay of cellular mRNA, in both the wild type and an NS1 deletion mutant.
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Zürcher et al. (2000) studied Influenza virus infection. Influenza virus infection vs. PKR(+) vs PKR(-) cells and wild-type vs mutant viruses was evaluated on Viral protein synthesis and decay of cellular protein synthesis. Influenza virus-induced protein synthesis shut-off and cellular mRNA decay occurred independently of PKR activity and the C-terminal sequences of the NS1 protein.
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