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

Wencheng Lin; Zhouyi Xu; Yiming Yan; Huanmin Zhang; Hongxin Li; Weiguo Chen; Feng Chen; Qingmei Xie

doi:10.3389/fmicb.2018.01089

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

Front Microbiol. 2018 May 25:9:1089. doi: 10.3389/fmicb.2018.01089. eCollection 2018.

Authors

Wencheng Lin^{1

2

3}, Zhouyi Xu¹, Yiming Yan¹, Huanmin Zhang⁴, Hongxin Li^{1

2

3}, Weiguo Chen^{1

2

3}, Feng Chen^{1

2

3}, Qingmei Xie^{1

2

3}

Affiliations

¹ Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, China.
² South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, China.
³ Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, China.
⁴ Avian Disease and Oncology Laboratory, USDA, Agriculture Research Service, East Lansing, MI, United States.

Abstract

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.

Keywords: ALV-J; NF-κB; immunosuppression; macrophage; type I interferon.