ArticleJournal of virology2009
Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Population immunity to clade 2.3.4.4b H5N1 is dominated by anti-neuraminidase antibodies.mBio · 2026Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses.International journal of molecular sciences · 2024Review
- Strategies of Influenza A Virus to Ensure the Translation of Viral mRNAs.Pathogens (Basel, Switzerland) · 2022Review
- Assessment of a quadrivalent nucleoside-modified mRNA vaccine that protects against group 2 influenza viruses.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- An In Vitro Microneutralization Assay for Influenza Virus Serology.Current protocols · 2022Article
- The Influenza A Virus Endoribonuclease PA-X Usurps Host mRNA Processing Machinery to Limit Host Gene Expression.Cell reports · 2019Article
- Host Shutoff in Influenza A Virus: Many Means to an End.Viruses · 2018Review
- Cross-reactive mouse monoclonal antibodies raised against the hemagglutinin of A/Shanghai/1/2013 (H7N9) protect against novel H7 virus isolates in the mouse model.Emerging microbes & infections · 2018Article
- Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response.Scientific reports · 2018Article
- hCLE/C14orf166, a cellular protein required for viral replication, is incorporated into influenza virus particles.Scientific reports · 2016Article
- Influenza Virus and Chromatin: Role of the CHD1 Chromatin Remodeler in the Virus Life Cycle.Journal of virology · 2016Article
- Middle East respiratory syndrome coronavirus ORF4b protein inhibits type I interferon production through both cytoplasmic and nuclear targets.Scientific reports · 2015Article
- An H10N8 influenza virus vaccine strain and mouse challenge model based on the human isolate A/Jiangxi-Donghu/346/13.Vaccine · 2015Article
- Specific residues of PB2 and PA influenza virus polymerase subunits confer the ability for RNA polymerase II degradation and virus pathogenicity in mice.Journal of virology · 2014Article
- Review
- CHD6, a cellular repressor of influenza virus replication, is degraded in human alveolar epithelial cells and mice lungs during infection.Journal of virology · 2013Article
- Cellular human CLE/C14orf166 protein interacts with influenza virus polymerase and is required for viral replication.Journal of virology · 2011Article
- DNA intercalator stimulates influenza transcription and virus replication.Virology journal · 2011Article
- Interferon antagonist NSs of La Crosse virus triggers a DNA damage response-like degradation of transcribing RNA polymerase II.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that infection with laboratory-passaged strains of influenza virus causes both specific degradation of the largest subunit of the RNA polymerase II complex (RNAP II) and inhibition of host cell transcription. When infection with natural human and avian isolates belonging to different antigenic subtypes was examined, we observed that all of these viruses efficiently induce the proteolytic process. To evaluate whether this process is a general feature of nonattenuated viruses, we studied the behavior of the influenza virus strains A/PR8/8/34 (PR8) and the cold-adapted A/Ann Arbor/6/60 (AA), which are currently used as the donor strains for vaccine seeds due to their attenuated phenotype. We have observed that upon infection with these strains, degradation of the RNAP II does not occur. Moreover, by runoff experiments we observe that PR8 has a reduced ability to inhibit cellular mRNA transcription. In addition, a hypervirulent PR8 (hvPR8) variant that multiplies much faster than standard PR8 (lvPR8) in infected cells and is more virulent in mice than the parental PR8 virus, efficiently induces RNAP II degradation. Studies with reassortant viruses containing defined genome segments of both hvPR8 and lvPR8 indicate that PA and PB2 subunits individually contribute to the ability of influenza virus to degrade the RNAP II. In addition, recently it has been reported that the inclusion of PA or PB2 from hvPR8 in lvPR8 recombinant viruses, highly increases their pathogenicity. Together, the data indicate that the capacity of the influenza virus to degrade RNAP II and inhibit the host cell transcription machinery is a feature of influenza A viruses that might contribute to their virulence.
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