ArticleJournal of virology2011
The measles virus V protein binds to p65 (RelA) to suppress NF-kappaB activity.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 77 citations in OpenAlex.
- Solution structure of the C-terminal domain of the measles virus V protein in its free form and mechanistic analysis of STAT2 targeting.Journal of virology · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Structure, Attachment and Transmembrane Internalisation of Peste Des Petits Ruminants Virus.Veterinary medicine and science · 2025Review
- Dengue virus NS5 degrades ERC1 during infection to antagonize NF-kB activation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- The Sphingolipid Inhibitors Ceranib-2 and SKI-II Reduce Measles Virus Replication in Primary Human Lymphocytes: Effects on mTORC1 Downstream Signaling.Frontiers in physiology · 2022Article
- Safe and effective two-in-one replicon-and-VLP minispike vaccine for COVID-19: Protection of mice after a single immunization.PLoS pathogens · 2021Article
- Peste des petits ruminants virus non-structural C protein inhibits the induction of interferon-β by potentially interacting with MAVS and RIG-I.Virus genes · 2021Article
- Advances in Antiviral Therapy for Subacute Sclerosing Panencephalitis.Molecules (Basel, Switzerland) · 2021Review
- Evasion of Host Antiviral Innate Immunity by Paramyxovirus Accessory Proteins.Frontiers in microbiology · 2021Review
- Seek and hide: the manipulating interplay of measles virus with the innate immune system.Current opinion in virology · 2020Review
- Phylogenomic Analysis of Two Co-Circulating Canine Distemper Virus Lineages in Colombia.Pathogens (Basel, Switzerland) · 2019Article
- Measles Encephalitis: Towards New Therapeutics.Viruses · 2019Review
- Review
- Extensive editing of cellular and viral double-stranded RNA structures accounts for innate immunity suppression and the proviral activity of ADAR1p150.PLoS biology · 2018Article
- MicroRNA-216a Inhibits NF-κB-Mediated Inflammatory Cytokine Production in Teleost Fish by Modulating p65.Infection and immunity · 2018Article
- Binding and entry of peste des petits ruminants virus into caprine endometrial epithelial cells profoundly affect early cellular gene expression.Veterinary research · 2018Article
- Measles vaccination: Threat from related veterinary viruses and need for continued vaccination post measles eradication.Human vaccines & immunotherapeutics · 2018Review
- Understanding the causes and consequences of measles virus persistence.F1000Research · 2018Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor κB (NF-κB) transcription factors are involved in controlling numerous cellular processes, including inflammation, innate and adaptive immunity, and cell survival. Here we show that the immunosuppressive measles virus (MV; Morbillivirus genus, Paramyxoviridae) has evolved multiple functions to interfere with canonical NF-κB signaling in epithelial cells. The MV P, V, and C proteins, also involved in preventing host cell interferon responses, were found to individually suppress NF-κB-dependent reporter gene expression in response to activation of the tumor necrosis factor (TNF) receptor, RIG-I-like receptors, or Toll-like receptors. NF-κB activity was most efficiently suppressed in the presence of V, while expression of P or C resulted in moderate inhibition. As indicated by reporter gene assays involving overexpression of the IκB kinase (IKK) complex, which phosphorylates the inhibitor of κB to liberate NF-κB, V protein targets a downstream step in the signaling cascade. Coimmunoprecipitation experiments revealed that V specifically binds to the Rel homology domain of the NF-κB subunit p65 but not of p50. Notably, the short C-terminal domain of the V protein, which is also involved in binding STAT2, IRF7, and MDA5, was sufficient for the interaction and for preventing reporter gene activity. As observed by confocal microscopy, the presence of V abolished nuclear translocation of p65 upon TNF-α stimulation. Thus, MV V appears to prevent NF-κB-dependent gene expression by retaining p65 in the cytoplasm. These findings reveal NF-κB as a key target of MV and stress the importance of the V protein as the major viral immune-modulatory factor.
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