This resulted in the so-called liquid-solid model (Kenkre et al
This resulted in the so-called liquid-solid model (Kenkre et al., 2007), which considers two extreme types of movement that this juveniles and adults perform in the field (freely diffusing and static); the home range itself does not vary. basis, contrary to what previous models predicted: a higher vole density does not necessary result in a higher contamination prevalence, nor in an increased number of humans reported having NE. Here, we advance a novel individual-based spatially-explicit model which takes into account the immunity provided by maternal antibodies and which simulates the spatial behavior of the host, both possible causes for this discrepancy that were not accounted for in previous models. We show that the reduced prevalence in peak years can be attributed to transient immunity, and that the density-dependent spatial vole behavior, i.e., the fact that home ranges are smaller in high density years, plays only a minor role. The applicability of the model is not limited to the study and prediction of PUUV (and NE) occurrence in Europe, as it could be easily adapted to model other rodent-borne diseases, either with indirect or direct transmission. = 0.76, 0.0001). This observation is usually supported by another impartial record: the number of human NE cases reported during the same time period. Although the number of cases can be expected to be proportional to bank vole density, it is not higher in a bank vole peak year but often even slightly lower than in increase years (Kallio et al., 2009). Even though an GS967 overall positive GS967 relationship between bank vole density and NE cases was found over a 14-years period, these data showed that increased density does not necessarily result in a higher GS967 NE incidence. In order to explain this discrepancy, Kallio et al. (2009, 2010) put forward possible explanations. They pointed at transient immunity through maternal antibodies (MatAb) as GS967 a potential cause. Infected females transfer MatAb to their offspring, which are then temporarily guarded against PUUV (Kallio et al., 2006b). In a peak year following an increase year, the seroprevalence in overwintered voles in spring approaches 100% (see Supplementary Material), and consequently most of the young born to these females should have maternal antibodies. This influx of maternally guarded newborns may delay transmission beyond the abundance peak, hence reducing the infection prevalence (Garnier et al., 2014). The presence of MatAb immunity in juveniles has been described in multiple hantavirus studies in both US and Europe (for an overview see Kallio et al., 2010). TEK Another explanation may be that this spatial behavior of bank voles varies with density. In Finland, it has been observed that in peak years, when the abundance is usually high already at the start of the breeding season, breeding female voles have smaller territories compared to low-abundance years (Koskela et al., 1999; Eccard et al., 2011a), probably to limit the number of (hostile) contacts. Such decrease in territory/home range size may affect contacts among voles, impede contamination transmission and may, if not in combination with the influx of immune newborns, be responsible for a reduced prevalence at higher abundances. The presence of acute and chronic infections in bank voles was also mentioned by Kallio et al. (2009) as a possible contributing factor. It is commonly assumed that viral shedding during the acute contamination period is usually higher compared to the chronic stage of contamination (Gavrilovskaya et al., 1990; Sauvage et al., 2003; Hardestam et al., 2008), though recently Voutilainen et al. (2015) showed that, at least for some transmission routes (urine and feces), the amount of virus shed possibly does not decrease over time. In this paper we tested.