In our co-morbidity mouse model of asthma and influenza, IL-10 was absent prior to CA04 infection, however, it was produced at later time points, i. e., day 7 p.i. Thus, it is reasonable to believe that IL-10 was expressed in response to tissue injury, with the lower levels observed in asthmatic mice correlating with reduced lung tissue pathology compared to non-asthmatic mice. The gene discussed is IL10; the disease is influenza.