DNA mismatch repair is required for the host innate response and controls cellular fate after influenza virus infection.
Identifieur interne : 000900 ( Main/Exploration ); précédent : 000899; suivant : 000901DNA mismatch repair is required for the host innate response and controls cellular fate after influenza virus infection.
Auteurs : Benjamin S. Chambers [États-Unis] ; Brook E. Heaton [États-Unis] ; Keiko Rausch [États-Unis] ; Rebekah E. Dumm [États-Unis] ; Jennifer R. Hamilton [États-Unis] ; Sara Cherry [États-Unis] ; Nicholas S. Heaton [États-Unis]Source :
- Nature microbiology [ 2058-5276 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux, Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Grippe humaine (génétique), Grippe humaine (immunologie), Humains, Immunité innée, Lignée cellulaire, Modèles animaux de maladie humaine, Régulation de l'expression des gènes, Réparation de mésappariement de l'ADN, Réplication virale, Réseaux de régulation génique, Souris, Stress oxydatif, Virus de la grippe A (immunologie), Virus de la grippe A (pathogénicité).
- MESH :
- génétique : Grippe humaine.
- immunologie : Grippe humaine, Virus de la grippe A.
- pathogénicité : Virus de la grippe A.
- Animaux, Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Humains, Immunité innée, Lignée cellulaire, Modèles animaux de maladie humaine, Régulation de l'expression des gènes, Réparation de mésappariement de l'ADN, Réplication virale, Réseaux de régulation génique, Souris, Stress oxydatif.
English descriptors
- KwdEn :
- A549 Cells, Animals, Cell Line, DNA Mismatch Repair, Disease Models, Animal, Dogs, Gene Expression Regulation, Gene Regulatory Networks, Humans, Immunity, Innate, Influenza A virus (immunology), Influenza A virus (pathogenicity), Influenza, Human (genetics), Influenza, Human (immunology), Madin Darby Canine Kidney Cells, Mice, Oxidative Stress, Virus Replication.
- MESH :
- genetics : Influenza, Human.
- immunology : Influenza A virus, Influenza, Human.
- pathogenicity : Influenza A virus.
- A549 Cells, Animals, Cell Line, DNA Mismatch Repair, Disease Models, Animal, Dogs, Gene Expression Regulation, Gene Regulatory Networks, Humans, Immunity, Innate, Madin Darby Canine Kidney Cells, Mice, Oxidative Stress, Virus Replication.
Abstract
Despite the cytopathic nature of influenza A virus (IAV) replication, we recently reported that a subset of lung epithelial club cells is able to intrinsically clear the virus and survive infection. However, the mechanisms that drive cell survival during a normally lytic infection remained unclear. Using a loss-of-function screening approach, we discovered that the DNA mismatch repair (MMR) pathway is essential for club cell survival of IAV infection. Repair of virally induced oxidative damage by the DNA MMR pathway not only allowed cell survival of infection, but also facilitated host gene transcription, including the expression of antiviral and stress response genes. Enhanced viral suppression of the DNA MMR pathway prevented club cell survival and increased the severity of viral disease in vivo. Altogether, these results identify previously unappreciated roles for DNA MMR as a central modulator of cellular fate and a contributor to the innate antiviral response, which together control influenza viral disease severity.
DOI: 10.1038/s41564-019-0509-3
PubMed: 31358986
Affiliations:
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Chambers</name><affiliation wicri:level="2"><nlm:affiliation>Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Heaton, Brook E" sort="Heaton, Brook E" uniqKey="Heaton B" first="Brook E" last="Heaton">Brook E. 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However, the mechanisms that drive cell survival during a normally lytic infection remained unclear. Using a loss-of-function screening approach, we discovered that the DNA mismatch repair (MMR) pathway is essential for club cell survival of IAV infection. Repair of virally induced oxidative damage by the DNA MMR pathway not only allowed cell survival of infection, but also facilitated host gene transcription, including the expression of antiviral and stress response genes. Enhanced viral suppression of the DNA MMR pathway prevented club cell survival and increased the severity of viral disease in vivo. Altogether, these results identify previously unappreciated roles for DNA MMR as a central modulator of cellular fate and a contributor to the innate antiviral response, which together control influenza viral disease severity.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Caroline du Nord</li><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Chambers, Benjamin S" sort="Chambers, Benjamin S" uniqKey="Chambers B" first="Benjamin S" last="Chambers">Benjamin S. Chambers</name></region><name sortKey="Cherry, Sara" sort="Cherry, Sara" uniqKey="Cherry S" first="Sara" last="Cherry">Sara Cherry</name><name sortKey="Dumm, Rebekah E" sort="Dumm, Rebekah E" uniqKey="Dumm R" first="Rebekah E" last="Dumm">Rebekah E. Dumm</name><name sortKey="Hamilton, Jennifer R" sort="Hamilton, Jennifer R" uniqKey="Hamilton J" first="Jennifer R" last="Hamilton">Jennifer R. Hamilton</name><name sortKey="Heaton, Brook E" sort="Heaton, Brook E" uniqKey="Heaton B" first="Brook E" last="Heaton">Brook E. Heaton</name><name sortKey="Heaton, Nicholas S" sort="Heaton, Nicholas S" uniqKey="Heaton N" first="Nicholas S" last="Heaton">Nicholas S. Heaton</name><name sortKey="Rausch, Keiko" sort="Rausch, Keiko" uniqKey="Rausch K" first="Keiko" last="Rausch">Keiko Rausch</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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