Interferon-induced inhibition of parainfluenza virus type 5; the roles of MxA, PKR and oligo A synthetase/RNase L
| Autor: | T.S. Carlos, D. F. Young, Silke Stertz, Richard E. Randall, Georg Kochs |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Gene Expression Regulation
Viral Myxovirus Resistance Proteins RNase P viruses MxA Biology Virus Replication Inclusion bodies Virus eIF-2 Kinase GTP-Binding Proteins Interferon Cell Line Tumor Virology Chlorocebus aethiops Endoribonucleases 2' 5'-Oligoadenylate Synthetase Protein biosynthesis medicine Animals Humans Parainflueza virus type 5 Vero Cells Messenger RNA PKR Protein kinase R Molecular biology Rubulavirus Vero cell Interferons OAS medicine.drug |
| Zdroj: | Virology. 363:166-173 |
| ISSN: | 0042-6822 |
| DOI: | 10.1016/j.virol.2007.01.014 |
| Popis: | We have previously reported that the addition of interferon (IFN) to the culture medium of Vero cells (which cannot produce IFN) that were infected with the CPI− strain of parainfluenza virus 5 (PIV5, formally known as SV5), that fails to block IFN signaling, rapidly induces alterations in the relative levels of virus mRNA and protein synthesis. In addition, IFN treatment also caused a rapid redistribution of virus proteins and enhanced the formation of cytoplasmic viral inclusion bodies. The most studied IFN-induced genes with known anti-viral activity are MxA, PKR and the Oligo A synthetase/RNase L system. We therefore examined the effects of these proteins on the replication cycle of PIV5. These studies revealed that while these proteins had some anti-viral activity against PIV5 they were not primarily responsible for the very rapid alteration in virus protein synthesis observed following IFN treatment, nor for the IFN-induced formation of virus inclusion bodies, in CPI− infected cells. |
| Databáze: | OpenAIRE |
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