AUTHOR=Mo Guodong , Fu Huali , Hu Bowen , Zhang Qihong , Xian Mingjian , Zhang Zihao , Lin Ling , Shi Meiqing , Nie Qinghua , Zhang Xiquan 

TITLE=SOCS3 Promotes ALV-J Virus Replication via Inhibiting JAK2/STAT3 Phosphorylation During Infection

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=11

YEAR=2021

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2021.748795

DOI=10.3389/fcimb.2021.748795

ISSN=2235-2988

ABSTRACT=<p>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 <italic>SOCS3</italic> in ALV-J infection and study how this gene affects ALV-J infection. In this study, we assessed the expression of the <italic>SOCS3</italic> gene <italic>in vivo</italic> and <italic>in vitro</italic>, and investigated the roles of <italic>SOCS3</italic> in ALV-J infection using overexpressed or interfered assays with the <italic>SOCS3</italic> in DF-1 cells. The results showed that the <italic>SOCS3</italic> expression of ALV-J infected chickens was different from uninfected chickens in the spleen, thymus and cecal tonsil. Further, <italic>SOCS3</italic> is mainly expressed in the nucleus as determined by immunofluorescence assay. Overexpression of <italic>SOCS3</italic> in DF-1 cells promoted the replication of ALV-J virus, and the expression of interferons (<italic>IFNα</italic> and <italic>INFβ</italic>), inflammatory factors (<italic>IL-6</italic> and <italic>TNFα</italic>) along with interferon-stimulating genes (<italic>CH25H</italic>, <italic>MX1</italic>, <italic>OASL</italic>, and <italic>ZAP</italic>). Conversely, interference of <italic>SOCS3</italic> showed the opposite results. We also observed that SOCS3 promoted ALV-J virus replication by inhibiting JAK2/STAT3 phosphorylation. In conclusion, <italic>SOCS3</italic> promotes ALV-J replication <italic>via</italic> 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.</p>