Open AccessProtein Synthesis Shut-Off Induced by Influenza Virus Infection Is Independent of PKR Activity
Author(s) -
Thomas Zürcher,
Rosa M. Marión,
Juan Ortı́n
Publication year - 2000
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.74.18.8781-8784.2000
Subject(s) - biology , shut down , virus , polyadenylation , protein biosynthesis , mutant , virology , messenger rna , cytoplasm , antiviral protein , viral replication , microbiology and biotechnology , influenza a virus , protein kinase r , rna , gene , protein kinase a , genetics , kinase , mitogen activated protein kinase kinase , computer science , operating system
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.