Since Sin Nombre hantavirus was first discovered in the US in 1993, the Centers for Disease Control and Prevention has classified it as an emerging infectious disease and sponsored longitudinal studies of the rodent reservoir host, the deer mouse. To quantitatively evaluate the proposed bottom-up trophic cascade hypothesis to explain Sin Nombre hantavirus outbreaks, we used a combination of mark-recapture analysis and mathematical models of 15 years of data from Montana.
Results/Conclusions
We show that mouse population dynamics in Montana are strongly correlated to precipitation and temperature with a 0 to 5 month lag. These changing environmental conditions alter the carrying capacity of the environment, which can lead to delayed density dependence in prevalence of the virus (with a lag of up to 16 months or more) in the mouse population and intermittent crossing of the critical host density necessary for hantavirus endemicity. This work helps shed some light on the notoriously difficult to understand dynamics of the virus, such as seemingly inverse density dependence in prevalence and sporadic disappearance of the virus from the local population. Since there is no effective treatment or vaccine for HPS, the most effective strategy is to take preventative measures. This quantitative understanding of the lags between environmental conditions and prevalence of the virus may allow us advance warning (up to 20 months or more) of increased risk to humans.