In addition to exuberant lung inflammation, secondary bacterial infections are often considered important contributors to influenza-related mortality [13, 14, 15] . Interestingly, we here demonstrate that the host response to bacterial products actually enhances the clearance of a viral pathogen (Fig. 1D) , just as we have shown for bacteria [16] . So, while viral infections may impair antibacterial interferon-c responses [15] , we observe no evidence that the response to the bacterial lysate impedes either type I or type II interferon signaling. Rather, the response to the bacterial products seems to reinforce protective antiviral events via vigorous interferon gene expression.