<i>Streptococcus pneumoniae</i>coinfection results in increased disease in a murine model of influenza B virus infection

Abstract Secondary Streptococcus pneumoniae (Spn) infection is commonly associated with increased hospitalization and death following seasonal influenza virus infection. The animal models of A (IAV) secondary Spn coinfection have described the morbidity mortality leading to several proposed mechanisms enhanced disease. Influenza B (IBV) causes 25% cases bacterial coinfection, yet little known about immune response IBV coinfection. Here, we established a mouse model study disease in singly coinfected animals define mechanism(s) Like IAV followed by inoculation resulted compared or alone. In primed mice, titers were early rapidly migrated lung. Analysis cytokines lung showed pro-inflammatory cytokine (TNF-α, IL-1β, IL-6) responses infection, which may be These data suggest that initiates innate are worsening Ongoing studies include analysis infiltrating cells during histopathologic complement mediators clinical NIH CIDER Contract #75N93021C00018