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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.

Original publication




Journal article


Arch Virol

Publication Date





701 - 705


Animals, Cell Line, Cricetinae, Cytopathogenic Effect, Viral, Equartevirus, Fibroblasts, Gene Expression Regulation, Viral, I-kappa B Kinase, Mice, Myeloid Differentiation Factor 88, NF-kappa B, Signal Transduction, Viral Proteins, Virus Replication