Aim. To understand the ecologic parameters of Sin Nombre virus (SNV; family Bunyaviridae, genus Hantavirus) infections in the deer mouse (Peromyscus maniculatus), environmental variables impacting the rodent populations, and the conditions under which SNV is amplified. This may help us understand the antecedents of human risk for developing hantavirus pulmonary syndrome (HPS) as a consequence of SNV infection. Method. Each 6 weeks, we trapped, measured, tagged, bled, and released rodents at three widely spaced sites in Colorado, USA: Fort Lewis (1994Lewis ( -2001, Molina (1994Molina ( -2001, and Pinyon Canyon Maneuver Site (1995)(1996)(1997)(1998)(1999)(2000)(2001). The ELISA method was used to test rodent blood samples for IgG antibody to SNV antigen. Results. Where rodent species richness was high, the prevalence of infection of deer mice (as determined by the presence of antibody) with SNV was low, and vice versa. There was a higher prevalence of antibody to SNV in male than in female rodents, and seasonal differences were observed in acquisition of SNV between male and female deer mice. Long-lived infected deer mice served as transseasonal, over-winter reservoirs for the virus, providing the mechanism for its survival. Conclusion. Prevalence of rodent infection appears to be associated with fluctuations in deer mouse populations and, indirectly, with timing and amount of precipitation and the resulting biologic events (a "trophic cascade"). Together with information regarding transseasonal maintenance of SNV, seasonal differences in acquisition of SNV between sexes, group foraging, and various other factors may expand our understanding of the risk factors for acquiring HPS. Taken together and applied, we anticipate developing methods for preventing this disease as well as diseases caused by other rodent-borne viruses
