NF-κB activation by equine arteritis virus is MyD88 dependent and promotes viral replication
NF-κB activation by equine arteritis virus is MyD88 dependent and promotes viral replication
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DOI：
10.1007/s00705-012-1515-4
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发表时间：
2013-03-01
影响因子：
2.7
通讯作者：
Baule, Claudia
中科院分区：
文献类型：
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作者：
Mottahedin, Amin;Paidikondala, Maruthibabu;Baule, Claudia
NF-κ B B是一个参与不同细胞功能和免疫应答的转录因子家族，是病毒的靶点。NF-κ B信号传导的机制及其在EAV复制中的作用尚未研究。我们证明，EAV感染BHK-21细胞激活NF-κ B，这种激活被发现是通过MyD 88途径介导的。感染NF-κ B信号传导缺陷的IKK β（-/-）鼠胚胎成纤维细胞（MEF），导致病毒滴度降低，细胞病变效应减少，病毒蛋白表达减少。这些发现暗示MyD 88通路在EAV诱导的NF-κ B活化中，并且表明NF-κ B活化对于EAV的有效复制是必需的。
NF-kappa B, a family of transcription factors involved in different cell functions and immune responses is targeted by viruses. The mechanism of NF-kappa B signalling and its role in replication of EAV have not been investigated. We demonstrate that EAV infection in BHK-21 cells activates NF-kappa B, and this activation was found to be mediated through the MyD88 pathway. Infection of IKK beta(-/-) murine embryo fibroblasts (MEFs), which are deficient in NF-kappa B 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-kappa B activation and suggest that NF-kappa B activation is essential for efficient replication of EAV.