Aside from IAV attenuation of the Sp-driven Th17 pathway, the IFN-γ response (both total and that produced by Sp-specific Th1 cells) was found to be increased in the coinfected mice compared to those with Sp infection alone (Fig. 2 and Fig. S2), which might contribute to decreased antibacterial immune responses and elevated susceptibility to secondary bacterial infection. The gene discussed is IFNG; the disease is bacterial infectious disease.