An increase in species diversity, in combination with an increase in the densities of individuals within those species, as we observed in this study, should also mean an increase in the number of predators of the rodent host species. It is reasonable to hypothesize that predators keep rodent numbers under control, in turn limiting pathogen spread both among rodents and into human populations, although it has been difficult to empirically support this hypothesis (35) . Our results suggest that predators control infection prevalence not by controlling the density of host species but instead by an unrelated mechanism, possibly encounter reduction. When predators are present in the ecosystem, host species should spend more time in the nest, in hiding, or within the familiarity of their territory, all to avoid predation and all likely to decrease intraspecies encounters. This hypothesis is supported by the fact that capture ratebut not density-was highest at site 1 during year 2 relative to all other parks (p<0.01), which means that deer mice were moving about and encountering traps more often. We hypothesize that when predation and competition are decreased or absent, for this small mammal community at a Simpson diversity index ≈0.43, a zoonotic release of predatory and competitive controls appears to have occurred, in which SNV infection prevalence increased drastically. This hypothesis would account for the lack of differences in infection prevalence rates at sites 2-5; although the Simpson index for these sites varied significantly; the threshold for zoonotic release had not been breached at any of those sites. Above the threshold level, sites would maintain a low level of infection, or perhaps locally lose infection altogether. In this study, SNV infection prevalence was either so low during some seasons at some sites as to be virtually undetectable by traditional trapping techniques or ephemerally absent. In particular, SNV was undetected or absent most often at the most diverse site (no SNV was detected in 8 of 12 seasons at site 5, in 6-7 seasons at sites 2-4, and in 1 season at site 1). Our system differs from the Lyme disease system, which depends on a vector that is not host specific (black-legged tick) to transmit the disease. Here, in contrast, presence of nonhost species in the small mammal community will not directly affect the transmission of SNV; instead, the behavior of members of the natural host species will be affected, decreasing SNV transmission rates among competent hosts through encounter reduction. Increased diversity in both the Lyme disease and SNV systems appears to lead to decreased disease prevalence, although the mechanisms differ. Another difference between the 2 systems is the threshold relationship between species diversity and SNV prevalence, which suggests that the shape of the dilution curve may be mechanism dependent and is the reason we proposed the term "zoonotic release." Given that many hantaviruses are hosted by generalist rodent species (i.e., those able to exploit a broad variety of ecological resources) that dominate ecosystems as species diversity decreases (e. Host density should likewise be considered a factor in this phenomenon because density increased before infection prevalence increased. However, the result of the logistic regression between density and infection prevalence, although significant, was marked by considerable overdispersion, suggesting that this was the wrong model, and its significance was greatly overestimated (32) . Additionally, at all parks deer mouse density increased but infection prevalence did not, clearly indicating that density is not the sole driver of infection prevalence in this system. A logistic regression with both density and mammal species diversity in the model showed similar overdispersion. Our results suggest that dependence on both density and frequency play a role in SNV transmission, which may be one of the reasons it has been so hard to determine their respective roles in the transmission of hantaviruses (36) . More extensive studies should therefore be undertaken wherein species diversity, density, and frequency of encounters are carefully measured to determine their respective roles in disease transmission.