ArticleJournal of virology2007
Importance of the anti-interferon capacity of Sendai virus C protein for pathogenicity in mice.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- USP24 is a cross-reactive DUB targeting MOV10 to regulate IFN-I production.Nature communications · 2026Article
- Article
- Review
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- Protocols to Manufacture an Oncolytic Measles Virus-Sensitive Immunocompetent Mouse Model of Medulloblastoma.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Respiratory Enterovirus (like Parainfluenza Virus) Can Cause Chronic Lung Disease if Protection by Airway Epithelial STAT1 Is Lost.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Identification of key genes and signaling pathways during Sendai virus infection in vitro.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2019Article
- An oncolytic measles virus-sensitive Group 3 medulloblastoma model in immune-competent mice.Neuro-oncology · 2018Article
- A Single Amino Acid Substitution within the Paramyxovirus Sendai Virus Nucleoprotein Is a Critical Determinant for Production of Interferon-Beta-Inducing Copyback-Type Defective Interfering Genomes.Journal of virology · 2018Article
- Structural analysis of the STAT1:STAT2 heterodimer revealed the mechanism of Sendai virus C protein-mediated blockade of type 1 interferon signaling.The Journal of biological chemistry · 2017Article
- Article
- Role of interferon regulatory factor 3-mediated apoptosis in the establishment and maintenance of persistent infection by Sendai virus.Journal of virology · 2013Article
- Nonstructural Nipah virus C protein regulates both the early host proinflammatory response and viral virulence.Journal of virology · 2012Article
- Expression of interferon-induced antiviral genes is delayed in a STAT1 knockout mouse model of Crimean-Congo hemorrhagic fever.Virology journal · 2012Article
- Recombinant vaccines against the mononegaviruses--what we have learned from animal disease controls.Virus research · 2011Review
- Virus-driven conditional expression of an interferon antagonist as a tool to circumvent host restriction.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Expression of the Sendai (murine parainfluenza) virus C protein alleviates restriction of measles virus growth in mouse cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Article
- Negative regulation of interferon-β gene expression during acute and persistent virus infections.PloS one · 2011Article
- Paramyxovirus assembly and budding: building particles that transmit infections.The international journal of biochemistry & cell biology · 2010Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Sendai virus (SeV) C protein blocks signal transduction of interferon (IFN), thereby counteracting the antiviral actions of IFN. Using HeLa cell lines expressing truncated or mutated SeV C proteins, we found that the C-terminal half has anti-IFN capacity, and that K(151)A, E(153)A, and R(154)A substitutions in the C protein eliminated this capacity. Here, we further created the mutant virus SeV Cm*, in which K(151)A, E(153)K, and R(157)L substitutions in the C protein were introduced without changing the amino acid sequence of overlapped P, V, and W proteins. SeV Cm* was found to lack anti-IFN capacity, as expected. While the growth rate and final yield of SeV Cm* were inferior to those of the wild-type SeV in IFN-responsive, STAT1-positive 2fTGH cells, SeV Cm* grew equivalently to the wild-type SeV in IFN-nonresponsive, STAT1-deficient U3A cells. SeV Cm* was thus shown to maintain multiplication capacity, except that it lacked anti-IFN capacity. Intranasally inoculated SeV Cm* could propagate in the lungs of STAT1(-/-) mice but was cleared from those of STAT1(+/+) mice without propagation. It was found that the anti-IFN capacity of the SeV C protein was indispensable for pathogenicity in mice. Conversely, the results show that the innate immunity contributed to elimination of SeV in early stages of infection in the absence of anti-IFN capacity.
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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.