ArticleJournal of virology2012
Viperin, MTAP44, and protein kinase R contribute to the interferon-induced inhibition of Bunyamwera Orthobunyavirus replication.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Viperin suppresses goose astrovirus type 2 replication through inhibition of viral RdRP activity.Veterinary research · 2026Article
- Review
- Viperin: A Multifunctional Protein in Antiviral Immunity and Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Bystander neuronal progenitors in forebrain organoids promote protective antiviral responses.Journal of neuroinflammation · 2025Article
- Article
- Suppression of Interferon Response and Antiviral Strategies of Bunyaviruses.Tropical medicine and infectious disease · 2024Review
- Innate immune response against vector-borne bunyavirus infection and viral countermeasures.Frontiers in cellular and infection microbiology · 2024Review
- Review
- On the Recognition of Natural Substrate CTP and Endogenous Inhibitor ddhCTP of SARS-CoV-2 RNA-Dependent RNA Polymerase: A Molecular Dynamics Study.Journal of chemical information and modeling · 2022Article
- Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes.Stem cell reports · 2022Article
- Viperin triggers ribosome collision-dependent translation inhibition to restrict viral replication.Molecular cell · 2022Article
- Article
- Structural Insight into the Substrate Scope of Viperin and Viperin-like Enzymes from Three Domains of Life.Biochemistry · 2021Article
- Review
- A Look intoViruses · 2021Review
- Crosstalk Between SUMO and Ubiquitin-Like Proteins: Implication for Antiviral Defense.Frontiers in cell and developmental biology · 2021Review
- The antiviral protein viperin interacts with the viral N protein to inhibit proliferation of porcine epidemic diarrhea virus.Archives of virology · 2020Article
- Viperin Reveals Its True Function.Annual review of virology · 2020Review
- Interferon-Induced Protein 44 and Interferon-Induced Protein 44-Like Restrict Replication of Respiratory Syncytial Virus.Journal of virology · 2020Article
- Viperin: An ancient radical SAM enzyme finds its place in modern cellular metabolism and innate immunity.The Journal of biological chemistry · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The first line of defense against viral infection is the interferon (IFN) response, which culminates in the expression of hundreds of proteins with presumed antiviral activity, and must be overcome by a virus for successful replication. The nonstructural NSs protein is the primary IFN antagonist encoded by Bunyamwera virus (BUNV), the prototype of the Orthobunyavirus genus and the family Bunyaviridae. The NSs protein interferes with RNA polymerase II-mediated transcription, thereby inhibiting cellular mRNA production, including IFN mRNAs. A recombinant virus, rBUNdelNSs, that is unable to express the NSs protein does not inhibit cellular transcription and is a strong IFN inducer. We report here that cells stimulated into the antiviral state by IFN-β treatment were protected against wild-type BUNV and rBUNdelNSs infection but addition of IFN-β after infection had little effect on the replication cycle of either virus. By screening a panel of cell lines that overexpressed individual IFN-stimulated genes, we found that protein kinase R (PKR), MTAP44, and particularly viperin appreciably restricted BUNV replication. The enzymatic activities of PKR and viperin were required for their inhibitory activities. Taken together, our data show that the restriction of BUNV replication mediated by IFN is an accumulated effect of at least three IFN-stimulated genes that probably act on different stages of the viral replication cycle.
Indexed as
Identifiers
What Socratic 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 Socratic graph.