NF-κB activation by equine arteritis virus is MyD88 dependent and promotes viral replication
Identifieur interne : 001399 ( Main/Exploration ); précédent : 001398; suivant : 001400NF-κB activation by equine arteritis virus is MyD88 dependent and promotes viral replication
Auteurs : Amin Mottahedin [Suède] ; Maruthibabu Paidikondala [Finlande] ; Harindranath Cholleti [Suède] ; Claudia Baule [Suède]Source :
- Archives of Virology [ 0304-8608 ] ; 2013-03-01.
Abstract
Abstract: NF-κB, a family of transcription factors involved in different cell functions and immune responses is targeted by viruses. The mechanism of NF-κB signalling and its role in replication of EAV have not been investigated. We demonstrate that EAV infection in BHK-21 cells activates NF-κB, and this activation was found to be mediated through the MyD88 pathway. Infection of IKKβ−/− murine embryo fibroblasts (MEFs), which are deficient in NF-κB signalling, resulted in lower virus titre, less cytopathic effect, and reduced expression of viral proteins. These findings implicate the MyD88 pathway in EAV-induced NF-κB activation and suggest that NF-κB activation is essential for efficient replication of EAV.
Url:
DOI: 10.1007/s00705-012-1515-4
Affiliations:
- Finlande, Suède
- East Middle Sweden, Svealand, Uusimaa
- Helsinki, Uppsala
- Université d'Helsinki, Université d'Uppsala
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<front><div type="abstract" xml:lang="en">Abstract: NF-κB, a family of transcription factors involved in different cell functions and immune responses is targeted by viruses. The mechanism of NF-κB signalling and its role in replication of EAV have not been investigated. We demonstrate that EAV infection in BHK-21 cells activates NF-κB, and this activation was found to be mediated through the MyD88 pathway. Infection of IKKβ−/− murine embryo fibroblasts (MEFs), which are deficient in NF-κB signalling, resulted in lower virus titre, less cytopathic effect, and reduced expression of viral proteins. These findings implicate the MyD88 pathway in EAV-induced NF-κB activation and suggest that NF-κB activation is essential for efficient replication of EAV.</div>
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