Journal of Virology, September 2000, p. 8781-8784, Vol. 74, No. 18
Centro Nacional de Biotecnología
(CSIC), Campus de Cantoblanco, 28049 Madrid, Spain
Received 25 February 2000/Accepted 26 June 2000
The role of PKR activity in influenza virus-induced cell shut-off
was studied by infection of PKR+ or PKR
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Protein Synthesis Shut-Off Induced by Influenza
Virus Infection Is Independent of PKR Activity

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.
*
Corresponding author. Mailing address: Centro Nacional
de Biotecnologia (CSIC), Campus de Cantoblanco, 28049 Madrid, Spain. Phone: 34 91 585 4557. Fax: 34 91 585 4506. E-mail:
jortin{at}cnb.uam.es.
Present address: GlaxoWellcome Medicines Research Centre,
Stevenage, Hertsfordshire SG1 2NY, United Kingdom.
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