ArticleThe Journal of general virology2013
ISG56/IFIT1 is primarily responsible for interferon-induced changes to patterns of parainfluenza virus type 5 transcription and protein synthesis.
Article in The Journal of general virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- IFIT1 is rapidly evolving and exhibits disparate antiviral activities across 11 mammalian orders.eLife · 2025Article
- The Cap-proximal secondary structures of the 5'UTRs of parainfluenza virus 5 mRNAs specify differential sensitivity to type I interferon and IFIT1.The Journal of general virology · 2025Article
- An MST-based assay reveals new binding preferences of IFIT1 for canonically and noncanonically capped RNAs.RNA (New York, N.Y.) · 2025Article
- Differential Contributions of Interferon Classes to Host Inflammatory Responses and Restricting Virus Progeny Production.Journal of proteome research · 2024Article
- Interferon inhibits a model RNA virus via a limited set of inducible effector genes.EMBO reports · 2023Article
- Structural aspects of hepatitis E virus.Archives of virology · 2022Review
- Review
- Interferon Control of Human Coronavirus Infection and Viral Evasion: Mechanistic Insights and Implications for Antiviral Drug and Vaccine Development.Journal of molecular biology · 2022Review
- Discovering antiviral restriction factors and pathways using genetic screens.The Journal of general virology · 2021Review
- Role ofJournal of veterinary science · 2021Article
- Review
- Article
- Direct Antiviral Activity of IFN-Stimulated Genes Is Responsible for Resistance to Paramyxoviruses in ISG15-Deficient Cells.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Innate Intracellular Antiviral Responses Restrict the Amplification of Defective Virus Genomes of Parainfluenza Virus 5.Journal of virology · 2020Article
- Human IFIT proteins inhibit lytic replication of KSHV: A new feed-forward loop in the innate immune system.PLoS pathogens · 2019Article
- The nonstructural proteins of Pneumoviruses are remarkably distinct in substrate diversity and specificity.Virology journal · 2017Article
- Identification of Interferon-Stimulated Gene Proteins That Inhibit Human Parainfluenza Virus Type 3.Journal of virology · 2016Article
- Article
- Human IFIT1 Inhibits mRNA Translation of Rubulaviruses but Not Other Members of the Paramyxoviridae Family.Journal of virology · 2016Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Interferon (IFN) induces an antiviral state in cells that results in alterations of the patterns and levels of parainfluenza virus type 5 (PIV5) transcripts and proteins. This study reports that IFN-stimulated gene 56/IFN-induced protein with tetratricopeptide repeats 1 (ISG56/IFIT1) is primarily responsible for these effects of IFN. It was shown that treating cells with IFN after infection resulted in an increase in virus transcription but an overall decrease in virus protein synthesis. As there was no obvious decrease in the overall levels of cellular protein synthesis in infected cells treated with IFN, these results suggested that ISG56/IFIT1 selectively inhibits the translation of viral mRNAs. This conclusion was supported by in vitro translation studies. Previous work has shown that ISG56/IFIT1 can restrict the replication of viruses lacking a 2'-O-methyltransferase activity, an enzyme that methylates the 2'-hydroxyl group of ribose sugars in the 5'-cap structures of mRNA. However, the data in the current study strongly suggested that PIV5 mRNAs are methylated at the 2'-hydroxyl group and thus that ISG56/IFIT1 selectively inhibits the translation of PIV5 mRNA by some as yet unrecognized mechanism. It was also shown that ISG56/IFIT1 is primarily responsible for the IFN-induced inhibition of PIV5.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.