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Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation

Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such ind...

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Detalles Bibliográficos
Autores principales: Lin, Wencheng, Xu, Zhouyi, Yan, Yiming, Zhang, Huanmin, Li, Hongxin, Chen, Weiguo, Chen, Feng, Xie, Qingmei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980975/
https://www.ncbi.nlm.nih.gov/pubmed/29887850
http://dx.doi.org/10.3389/fmicb.2018.01089
Descripción
Sumario:Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such induction is still unclear. Here, we report that the inhibitory effect of ALV-J infection on type I interferon expression is associated with the down-regulation of transcriptional regulator NF-κB in host cells. We found that ALV-J possess the inhibitory effect on type I interferon production in HD11 cells and that ALV-J causes the up-regulation of IκBα and down-regulation of NF-κB p65, and that ALV-J blocks the phosphorylation of IκBα on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J.