Promotes ALV-J Virus ReplicationInhibiting JAK2/STAT3 Phosphorylation During Infection.

Abstract

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 ofin ALV-J infection and study how this gene affects ALV-J infection. In this study, we assessed the expression of thegeneand, and investigated the roles ofin ALV-J infection using overexpressed or interfered assays with thein DF-1 cells. The results showed that theexpression 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 ofin 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 ofshowed the opposite results. We also observed that SOCS3 promoted ALV-J virus replication by inhibiting JAK2/STAT3 phosphorylation. In conclusion,promotes ALV-J replicationinhibiting 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.