An evaluation of the immune response of deer mice to Sin Nombre virus
An evaluation of the immune response of deer mice to Sin Nombre virus
复制标题
鹿鼠对 Sin Nombre 病毒免疫反应的评估
DOI:
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复制
发表时间:
2012
期刊:
影响因子:
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通讯作者:
E. Lehmer
中科院分区:
文献类型:
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作者:
Ashley Kelly;E. Molinar;Joni Ghachu;Lacey Hart;Colleen;O’Brien;K. Wright;T. Schountz;Cathy Hartney;E. Lehmer
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 SNVand, 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 HPSmortality. 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.
影响因子:
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作者:
G. Gleich;C. Adolphson
通讯作者:
G. Gleich;C. Adolphson
影响因子:
6
作者:
S. Zaki;P. Greer;L. Coffield;C. Goldsmith;K. B. Nolte;K. Foucar;R. Feddersen;R. Zumwalt;G. Miller;Ali S Khan;P. Rollin;T. Ksiazek;S. Nichol;B. Mahy;C. Peters
通讯作者:
S. Zaki;P. Greer;L. Coffield;C. Goldsmith;K. B. Nolte;K. Foucar;R. Feddersen;R. Zumwalt;G. Miller;Ali S Khan;P. Rollin;T. Ksiazek;S. Nichol;B. Mahy;C. Peters