Hantaviruses are found throughout the world, but the Sin Nombre strain is highly prevalent in the Southwest region of the United States. Sin Nombre virus (SNV) is a rodent-borne zoonotic pathogen that causes Hantavirus Pulmonary Syndrome (HPS) in humans, a disease with exceptionally high (~40%) mortality rates. The primary reservoir for SNV is the deer mouse (Peromyscus maniculatus). Once infected with SNV, deer mice remain infected for life but exhibit few symptoms. Despite these apparently asymptomatic infections, the extent to which SNV infection impacts the ability of deer mice to respond to other pathogens is unknown. Likewise, it is unknown how the immune response to SNV changes across seasons within individual deer mice. Fluctuations in immunocompetence could have important implications for human health, as deer mice with suppressed immune systems are more likely to shed SNV in urine and feces, thus increasing the risk of human infection. Therefore, the objective of our study was to determine whether deer mice differentially allocate immune resources during seasonally stressful periods, like reproduction. As part of this study, we conducted a capture-mark-recapture study in which we live-trapped three populations of deer mice monthly from April to November 2011. Upon capture, we collected blood samples from individual deer mice and recorded basic demographic information (reproductive status, sex, age, body mass, presence of ectoparasites). In the lab we used blood samples to screen for infection with SNV. We determined innate immunocompetence by culturing deer mouse serum with E-coli and quantifying the number of E-coli colonies killed by antibacterial agents within the serum. Our results indicated that the immunocompetence of deer mice infected with SNV is compromised due to seasonal stressors. This suggests when confronted with other pathogens, infected deer mice will have a weakened immune response in comparison to their non-infected counterparts.
