In conclusion, our data support the hypothesis that influenza influences IPD risk by enhancing pneumococcal invasion in colonized individuals, but has little effect on the transmission dynamics of pneumococcal infection. We suggest that the mechanism for such an effect might be influenza-related alterations at the level of the respiratory epithelium [27] . These effects appear distinct from those of ambient environmental effects, although the effect of increased UV radiation in reducing IPD risk that we had previously reported in a study performed in Philadelphia needs further study [22] . These findings have important implications for disease control policy, and suggest that improved efficacy of influenza vaccines [38] , and novel vaccination strategies that more effectively control influenza by vaccinating younger individuals [33] , could have important effects in reducing IPD as well. Although they found wintertime peaks for infections with both pathogens, there was no correlation between the seasonal wave forms for influenza and IPD. That is, there was no relationship between the seasonal patterns of the two infections. By contrast, two of the statistical methods used to test hypothesis 2 revealed a short-term association between infections with influenza and with IPD. Moreover, the third statistical method (the Granger causality Wald test, a type of time-series analysis) provided evidence that data collected at intervals on influenza can be used to predict peaks in IPD infections.