Nellie McLean, Ashley Kelly, Edlin Molinar, Joni Ghachu, Lacey Hart, Colleen O'Brien, Kimberly Wright, Tony Schountz, Cathy Hartney, Erin M. Lehmer
BIOS 83 (3), 81-89, (1 September 2012) https://doi.org/10.1893/0005-3155-83.3.81
KEYWORDS: immunity
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.