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Common respiratory viruses cause seasonal epidemics in sequential patterns.The underlying mechanisms for this pattern have been debated for some time. Forinfluenza, contenders include temperature, humidity, and vitamin D levels.While such seasonal drivers may be sufficient to explain midwinter peaking itis unclear if other respiratory viruses peaking in spring, summer, or fall haveindividual environmental drivers. Here we present a dynamic model ofinteracting diseases, in an effort to explain observed seasonal patternswithout requiring multiple seasonal drivers. Our model extends the classicalSIRS-model to include multiple diseases that interact via a short-lasting,non-specific immunity component. This temporal protection is triggered byexposure to any epidemic disease and lasts only a couple of weeks. We show thatthe inhibiting disease-interaction allows recurrent epidemic behaviour withoutany seasonal driving. In the presence of a single seasonal driver our modelparsimoniously predicts epidemic patterns such as sequentially occurringepidemic diseases. We also present a two-disease simulation reproducingmultiple features observed in time series of parainfluenza strains PIV-3 andbiennial PIV-1 epidemic patterns. Complex epidemic patterns of seasonaldiseases may be explained by non-specific innate or cloub cell (T-cell)mediated immune responses that result in interaction between unrelatedrespiratory epidemic diseases.

Could short-lasting non-specific immunity explain seasonal spacing of epidemic diseases?