Search

Sin Nombre virus (SNV) causes hantavirus pulmonary syndrome (HPS) in humans, a disease with high (∼36%) mortality. Deer mice (Peromyscus maniculatus) are the primary host of SNV and, unlike humans, deer mice infected with SNV have few overt signs of disease. The reasons for such mild infections in deer mice have not been well studied; however, this information may be useful in uncovering therapies that could reduce human HPS mortality. Therefore, the objective of this study was to evaluate the immune response of deer mice to SNV by examining their patterns of white blood cell production. We quantified the number of lymphocytes, eosinophils, basophils, neutrophils, and monocytes produced by wild deer mice in both the early and late stages of SNV infection. Deer mice captured in the early season had greater basophil, lymphocyte, and eosinophil levels compared to deer mice captured in the late season. Conversely, monocyte levels were greater in deer mice captured in the late season. SNV infection status appeared to influence production of both neutrophils and monocytes, with SNV-infected mice having greater neutrophil levels but lower monocyte levels than uninfected mice. Collectively, the results seem to support the notion that immune stressors faced by wild deer mice shift from early to late season, and these differences are reflected by differential leukocyte production that occurs across seasons. Furthermore, our results indicate some potential differences between wild deer mice and lab-bred deer mice, as well as some possible similarities between wild deer mice and humans in their immune responses to SNV infection.

We examined how climate-mediated forest dieback regulates zoonotic disease prevalence using the relationship between sudden aspen decline (SAD) and Sin Nombre virus (SNV) as a model system. We compared understory plant community structure, small mammal community composition, and SNV prevalence on 12 study sites within aspen forests experiencing levels of SAD ranging from10.0% crown fade to95.0% crown fade. Our results show that sites with the highest levels of SAD had reduced canopy cover, stand density, and basal area, and these differences were reflected by reductions in understory vegetation cover. Conversely, sites with the highest levels of SAD had greater understory standing biomass, suggesting that vegetation on these sites was highly clustered. Changes in forest and understory vegetation structure likely resulted in shifts in small mammal community composition across the SAD gradient, as we found reduced species diversity and higher densities of deer mice, the primary host for SNV, on sites with the highest levels of SAD. Sites with the highest levels of SAD also had significantly greater SNV prevalence compared to sites with lower levels of SAD, which is likely a result of their abundance of deer mice. Collectively, results of our research provide strong evidence to show SAD has considerable impacts on vegetation community structure, small mammal density and biodiversity and the prevalence of SNV.