ArticleJournal of virology2011
A recombinant measles virus unable to antagonize STAT1 function cannot control inflammation and is attenuated in rhesus monkeys.
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 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 53 citations in OpenAlex.
- Efficient and reliable measles reprogramming platform for the generation of human iPSC.Molecular therapy. Advances · 2026Article
- 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
- From data to publication in a browser with BRC-Analytics: Evolutionary dynamics of coding overlaps in measles virus.bioRxiv : the preprint server for biology · 2025Article
- Reprogramming viral immune evasion for a rational design of next-generation vaccines for RNA viruses.Frontiers in immunology · 2023Review
- Article
- Investigating the Interaction between Negative Strand RNA Viruses and Their Hosts for Enhanced Vaccine Development and Production.Vaccines · 2021Review
- Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene.Virus evolution · 2021Review
- Engineering and combining oncolytic measles virus for cancer therapy.Cytokine & growth factor reviews · 2020Review
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- The Measles Virus V Protein Binding Site to STAT2 Overlaps That of IRF9.Journal of virology · 2020Article
- Seek and hide: the manipulating interplay of measles virus with the innate immune system.Current opinion in virology · 2020Review
- Measles Resurgence and Drug Development.Current opinion in virology · 2020Review
- Review
- Receptor-mediated cell entry of paramyxoviruses: Mechanisms, and consequences for tropism and pathogenesis.The Journal of biological chemistry · 2020Review
- Antagonism of STAT1 by Nipah virus P gene products modulates disease course but not lethal outcome in the ferret model.Scientific reports · 2019Article
- Measles Encephalitis: Towards New Therapeutics.Viruses · 2019Review
- Life-Threatening Infections Due to Live-Attenuated Vaccines: Early Manifestations of Inborn Errors of Immunity.Journal of clinical immunology · 2019Review
- Measles Virus Bearing Measles Inclusion Body Encephalitis-Derived Fusion Protein Is Pathogenic after Infection via the Respiratory Route.Journal of virology · 2019Article
- Cyclical adaptation of measles virus quasispecies to epithelial and lymphocytic cells: To V, or not to V.PLoS pathogens · 2019Article
- Nectin-4 Interactions Govern Measles Virus Virulence in a New Model of Pathogenesis, the Squirrel Monkey (Saimiri sciureus).Journal of virology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Measles remains a leading cause of death worldwide among children because it suppresses immune function. The measles virus (MV) P gene encodes three proteins (P, V, and C) that interfere with innate immunity, controlling STAT1, STAT2, mda5, and perhaps other key regulators of immune function. We identified here three residues in the shared domain of the P and V proteins-tyrosine 110, valine 112, and histidine 115-that function to retain STAT1 in the cytoplasm and inhibit interferon transcription. This information was used to generate a recombinant measles virus unable to antagonize STAT1 function (STAT1-blind MV) differing only in these three residues from a wild-type strain of well-defined virulence. This virus was used to assess the relevance of P and V interactions with STAT1 for virulence in primates. When a group of six rhesus monkeys (Macaca mulatta) was inoculated intranasally with STAT1-blind MV, viremia was short-lived, and the skin rash and other clinical signs observed with wild-type MV were absent. The STAT1-blind virus less efficiently controlled the inflammatory response, as measured by enhanced transcription of interleukin-6 and tumor necrosis factor alpha in peripheral blood mononuclear cells from infected hosts. Importantly, neutralizing antibody titers and MV-specific T-cell responses were equivalent in hosts infected with either virus. These findings indicate that efficient MV interactions with STAT1 are required to sustain virulence in a natural host by controlling the inflammatory response against the virus. They also suggest that selectively STAT1-blind MV may have utility as vectors for targeted oncolysis and vaccination.
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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.