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TNFα Impairs Rhabdoviral Clearance by Inhibiting the Host Autophagic Antiviral Response

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dc.contributor.authorRaquel Espín-Palazón
dc.contributor.authorEspín Palazón, Raquel
dc.contributor.authorMartínez López, Alicia
dc.contributor.authorRoca Soler, Francisco José
dc.contributor.authorLópez Muñoz, Azucena
dc.contributor.authorTyrkalska, Syilwia Dominika
dc.contributor.authorCandel Camacho, Sergio
dc.contributor.authorGarcía Moreno, Diana
dc.contributor.authorFalco, Alberto
dc.contributor.authorMeseguer, José
dc.contributor.authorEstepa, Amparo
dc.contributor.authorMulero Méndez, Victoriano Francisco
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2026-02-25T16:30:27Z
dc.date.available2026-02-25T16:30:27Z
dc.date.copyright© 2016 Espín-Palazón et al.
dc.date.issued2016-06-28
dc.description.abstractTNFα is a pleiotropic pro-inflammatory cytokine with a key role in the activation of the immune system to fight viral infections. Despite its antiviral role, a few viruses might utilize the host produced TNFα to their benefit. Some recent reports have shown that anti-TNFα therapies could be utilized to treat certain viral infections. However, the underlying mechanisms by which TNFα can favor virus replication have not been identified. Here, a rhabdoviral infection model in zebrafish allowed us to identify the mechanism of action by which Tnfa has a deleterious role for the host to combat certain viral infections. Our results demonstrate that Tnfa signals through its receptor Tnfr2 to enhance viral replication. Mechanistically, Tnfa does not affect viral adhesion and delivery from endosomes to the cytosol. In addition, the host interferon response was also unaffected by Tnfa levels. However, Tnfa blocks the host autophagic response, which is required for viral clearance. This mechanism of action provides new therapeutic targets for the treatment of SVCV-infected fish, and advances our understanding of the previously enigmatic deleterious role of TNFα in certain viral infections.
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dc.format.extent20
dc.identifier.citationPLoS Pathog, 2016, Vol. 12(6): e1005699
dc.identifier.doihttps://doi.org/10.1371/journal.ppat.1005699
dc.identifier.eissn1553-7374
dc.identifier.issn1553-7366
dc.identifier.urihttp://hdl.handle.net/10201/213621
dc.languageeng
dc.publisherPublic Library of Science
dc.relationThis study was funded by: MINECO BIO2011-23400 (VM), MINECO CSD2007-00002 (VM), MINECO BIO2014-52655-R (VM), MINECO AGL2014-51773-C3-1-R (AE), and Fondos Europeos de Desarrollo Regional (FEDER) (VM AE).
dc.relation.publisherversionhttps://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005699
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.odsObjetivo 12: Producción y consumo sostenibles
dc.titleTNFα Impairs Rhabdoviral Clearance by Inhibiting the Host Autophagic Antiviral Response
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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