Location: Endemic Poultry Viral Diseases ResearchTitle: Avian leukosis virus subgroup J attenuates type I interferon production through blocking IkB phosphorylation
|LIN, WENCHENG - Guangdong Testing Institute Of Product Quality Supervision|
|XU, ZHOUYI - South China Agricultural University|
|YAN, YIMING - South China Agricultural University|
|LI, HONGXIN - South China Agricultural University|
|CHEN, WEIGUO - South China Agricultural University|
|CHEN, FENG - South China Agricultural University|
|XIE, QINGMEI - South China Agricultural University|
Submitted to: Frontiers in Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/7/2018
Publication Date: 5/25/2018
Citation: Lin, W., Xu, Z., Yan, Y., Zhang, H., Li, H., Chen, W., Chen, F., Xie, Q. 2018. Avian leukosis virus subgroup J attenuates type I interferon production through blocking IkB phosphorylation. Frontiers in Microbiology. 9(1089):1-13. https://doi.org/10.3389/fmicb.2018.01089.
Interpretive Summary: The subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus. ALV-J remains a critical threat to the poultry industry worldwide. ALV-J infection causes immunosuppression and enhances susceptibility to secondary infection, which generally results in severe economic losses. There are rich literatures on ALV-J study. The molecular mechanism, however, on how the infection of this virus exactly leads to pathogenicity remains poorly understood. This study demonstrated that ALV-J infection leads to cytokines, a broad and loose category of small proteins (~5–20 kDa) that are important in governing and coordinating basic activities of cells, production alteration and subsequently blocking normal phosphorylation processes in specific amino acids. The findings advanced the basic understanding on ALV-J pathogenesis and provided essential new information that would facilitate future development of improved strategies in control of ALV-J infection in poultry.
Technical 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-'B 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 I'Ba and down-regulation of NF-'B p65, and that ALV-J blocks the phosphorylation of I'Ba on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J.