Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, China.
Guangdong Provincial Key Lab of AgroAnimal Genomics and Molecular Breeding and Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture and Rural Affairs, Guangzhou, China.
Front Cell Infect Microbiol. 2021 Sep 10;11:748795. doi: 10.3389/fcimb.2021.748795. eCollection 2021.
Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and neoplastic diseases in poultry. Cytokine signal-transduction inhibitor molecule 3 (SOCS3) is an important negative regulator of the JAK2/STAT3 signaling pathway and plays certain roles in ALV-J infection. It is of significance to confirm the roles of in ALV-J infection and study how this gene affects ALV-J infection. In this study, we assessed the expression of the gene and , and investigated the roles of in ALV-J infection using overexpressed or interfered assays with the in DF-1 cells. The results showed that the expression of ALV-J infected chickens was different from uninfected chickens in the spleen, thymus and cecal tonsil. Further, is mainly expressed in the nucleus as determined by immunofluorescence assay. Overexpression of in DF-1 cells promoted the replication of ALV-J virus, and the expression of interferons ( and ), inflammatory factors ( and ) along with interferon-stimulating genes (, , , and ). Conversely, interference of showed the opposite results. We also observed that SOCS3 promoted ALV-J virus replication by inhibiting JAK2/STAT3 phosphorylation. In conclusion, promotes ALV-J replication inhibiting the phosphorylation of the JAK2/STAT3 signaling pathway. These results would advance further understanding of the persistent infection and the viral immune evasion of the ALV-J virus.
禽白血病病毒亚群 J（ALV-J）是一种致瘤性逆转录病毒，可引起家禽免疫抑制和肿瘤性疾病。细胞因子信号转导抑制因子 3（SOCS3）是 JAK2/STAT3 信号通路的重要负调控因子，在 ALV-J 感染中发挥一定作用。确认在 ALV-J 感染中的作用，研究该基因如何影响 ALV-J 感染，具有重要意义。本研究通过检测 ALV-J 感染鸡脾脏、胸腺和盲肠扁桃体中 SOCS3 基因和 的表达，以及利用过表达和干扰 SOCS3 基因在 DF-1 细胞中对 ALV-J 感染的影响，研究 SOCS3 在 ALV-J 感染中的作用。结果显示，感染 ALV-J 的鸡与未感染的鸡相比，其脾脏、胸腺和盲肠扁桃体中的 表达存在差异。进一步的免疫荧光检测结果表明，SOCS3 主要定位于细胞核。在 DF-1 细胞中过表达 SOCS3 可促进 ALV-J 病毒的复制，同时上调干扰素（和）、炎症因子（和）及干扰素刺激基因（、、、）的表达；干扰 SOCS3 的表达则呈现相反的结果。此外，SOCS3 通过抑制 JAK2/STAT3 磷酸化促进 ALV-J 病毒的复制。综上所述，SOCS3 通过抑制 JAK2/STAT3 信号通路的磷酸化促进 ALV-J 的复制。这些结果将有助于进一步了解 ALV-J 病毒的持续感染和病毒免疫逃逸机制。
