ArticleThe Journal of biological chemistry2011
Interferon antagonist NSs of La Crosse virus triggers a DNA damage response-like degradation of transcribing RNA polymerase II.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 96 citations in OpenAlex.
- Emerging threat of Oropouche virus: Clinical features, experimental models, and virulence.Virulence · 2026Review
- The La Crosse virus M segment determines virus isolate cell-to-cell spread and virulence.bioRxiv : the preprint server for biology · 2026Article
- Oropouche Virus: Comparative Study of Two Strains Reveals Distinct Innate Immunity Modulation.Viruses · 2026Article
- Alphavirus M1 disrupts super-enhancer-driven oncogenic transcription via non-structural protein NSP2 in osteosarcoma.Nature communications · 2026Article
- Review
- Oropouche virus NSs protein suppresses host transcription by targeting the RNA polymerase II RPB1 protein.Journal of virology · 2025Article
- Orthobunyavirus neurovirulence is a complex trait involving all three genome segments.bioRxiv : the preprint server for biology · 2025Article
- NSs: the multifaceted bunyavirus virulence factor.Npj viruses · 2025Review
- Bystander neuronal progenitors in forebrain organoids promote protective antiviral responses.Journal of neuroinflammation · 2025Article
- Suppression of Interferon Response and Antiviral Strategies of Bunyaviruses.Tropical medicine and infectious disease · 2024Review
- Human coronavirus NL63 nsp1 induces degradation of RNA polymerase II to inhibit host protein synthesis.PLoS pathogens · 2024Article
- Role of CARD9 in Cell- and Organ-Specific Immune Responses in Various Infections.International journal of molecular sciences · 2024Review
- Innate immune response against vector-borne bunyavirus infection and viral countermeasures.Frontiers in cellular and infection microbiology · 2024Review
- Differential role of NSs genes in the neurovirulence of two genogroups of Akabane virus causing postnatal encephalomyelitis.Archives of virology · 2023Article
- mRNA 3'UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus.Nature communications · 2023Article
- La Crosse Virus Neuroinvasive Disease in Children: A Contemporary Analysis of Clinical/Neurobehavioral Outcomes and Predictors of Disease Severity.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Article
- Regulation of host factor γ-H2AX level and location by enterovirus A71 for viral replication.Virulence · 2022Article
- An Overview of the Infectious Cycle of Bunyaviruses.Viruses · 2022Review
- Article
- Differences in neuroinvasion and protective innate immune pathways between encephalitic California Serogroup orthobunyaviruses.PLoS pathogens · 2022Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
La Crosse encephalitis virus (LACV) is a mosquito-borne member of the negative-strand RNA virus family Bunyaviridae. We have previously shown that the virulence factor NSs of LACV is an efficient inhibitor of the antiviral type I interferon system. A recombinant virus unable to express NSs (rLACVdelNSs) strongly induced interferon transcription, whereas the corresponding wt virus (rLACV) suppressed it. Here, we show that interferon induction by rLACVdelNSs mainly occurs through the signaling pathway leading from the pattern recognition receptor RIG-I to the transcription factor IRF-3. NSs expressed by rLACV, however, acts downstream of IRF-3 by specifically blocking RNA polymerase II-dependent transcription. Further investigations revealed that NSs induces proteasomal degradation of the mammalian RNA polymerase II subunit RPB1. NSs thereby selectively targets RPB1 molecules of elongating RNA polymerase II complexes, the so-called IIo form. This phenotype has similarities to the cellular DNA damage response, and NSs was indeed found to transactivate the DNA damage response gene pak6. Moreover, NSs expressed by rLACV boosted serine 139 phosphorylation of histone H2A.X, one of the earliest cellular reactions to damaged DNA. However, other DNA damage response markers such as up-regulation and serine 15 phosphorylation of p53 or serine 1524 phosphorylation of BRCA1 were not triggered by LACV infection. Collectively, our data indicate that the strong suppression of interferon induction by LACV NSs is based on a shutdown of RNA polymerase II transcription and that NSs achieves this by exploiting parts of the cellular DNA damage response pathway to degrade IIo-borne RPB1 subunits.
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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.