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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Published inFrontiers in microbiology Vol. 9; p. 1089
Main Authors Lin, Wencheng, Xu, Zhouyi, Yan, Yiming, Zhang, Huanmin, Li, Hongxin, Chen, Weiguo, Chen, Feng, Xie, Qingmei
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 25.05.2018
Subjects
ALV-J
immunosuppression
macrophage
Microbiology
NF-κB
type I interferon
type I interferon
NF-κB
immunosuppression
macrophage
ALV-J
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Summary: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.
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This article was submitted to Virology, a section of the journal Frontiers in Microbiology
Edited by: Akio Adachi, Kansai Medical University, Japan
Reviewed by: Yoshinao Kubo, Nagasaki University, Japan; Masaaki Miyazawa, Kindai University, Japan; Michael Teng, University of South Florida, United States
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2018.01089