This data highlights the importance of SOCS1 and SOCS3 in H5N1 virus-induced innate immune response, suggesting a possible relationship between hyper-induction of these negative regulators of IFN signaling in the initial rounds of virus replication, with a concomitant decreased expression in antiviral genes leading to an increase in viral load at the later stage of infection that could contribute to the pathogenesis of H5N1 virus infection. The gene discussed is SOCS3; the disease is infection.