CNTFRα Facilitates Recombinant ALV Replication Through PI3K/Akt-Associated Regulation of Apoptosis and Inflammatory Responses

Avian leukosis virus (ALV) is a highly immunosuppressive and oncogenic retrovirus that poses a substantial threat to global poultry health. An increasing number of naturally occurring recombinant ALV strains belonging to different subgroups have been identified in recent field outbreaks. In this study, CNTFRα expression was increased following ALV-FJ15TH0 infection in vivo and in vitro. The relationship between CNTFRα expression and viral antigen levels warrants further investigation. Here, we demonstrate that CNTFRα overexpression increases ALV-FJ15TH0 strain antigen expression in DF-1 cells. CNTFRα overexpression was also associated with increased phosphorylation of components of the PI3K/Akt signaling pathway, together with changes in apoptosis, cellular invasiveness, cell viability, and cell-cycle progression. Furthermore, CNTFRα overexpression modulated inflammatory cytokine expression in a time-dependent manner, with different effects on IFN-α, IFN-β, TNF-α, and IL-1β depending on the time point. Collectively, these findings suggest that CNTFRα is associated with ALV-FJ15TH0 antigen expression and cellular responses in DF-1 cells, potentially involving PI3K/Akt signaling. However, the causal role of CNTFRα in ALV pathogenesis in vivo remains to be established.