TY - JOUR
T1 - Sin Nombre hantavirus decreases survival of male deer mice
AU - Luis, Angela D.
AU - Douglass, Richard J.
AU - Hudson, Peter J.
AU - Mills, James N.
AU - Bjørnstad, Ottar N.
N1 - Funding Information:
Acknowledgments We thank Dave Cameron and Dana Ranch Inc. and the Confederated Salish and Kootenai Tribes at Polson for unlimited access to their properties. S. Carver, K. Hughes, K Coffin, B. Lonner, D. Waltee, R. Van Horn, W. Semmens, and T. Wilson provided valuable assistance in the field. S. Zanto provided serologic testing at the Montana State Department of Public Health and Human Services Laboratory; P. Rollin and A. Comer arranged serologic testing at the Special Pathogens Branch Laboratory, US Centers for Disease Control and Prevention. ADL was supported in part by the Academic Computing Fellowship of the Pennsylvania State University. Financial support was provided by the National Institute of Health (NIH) grant # P20RR16455-05 from the INBRE—BRIN program and the US Centers for Disease Control and Prevention, Atlanta, GA, through cooperative agreement # US3/CCU813599, and the Research and Policy for Infectious Disease Dynamics (RAPIDD) program of the Science and Technology Directorate (Department of Homeland Security) and the Fogarty International Center (NIH).
PY - 2012/6
Y1 - 2012/6
N2 - How pathogens affect their hosts is a key question in infectious disease ecology, and it can have important influences on the spread and persistence of the pathogen. Sin Nombre virus (SNV) is the etiological agent of hantavirus pulmonary syndrome (HPS) in humans. A better understanding of SNV in its reservoir host, the deer mouse, could lead to improved predictions of the circulation and persistence of the virus in the mouse reservoir, and could help identify the factors that lead to increased human risk of HPS. Using mark-recapture statistical modeling on longitudinal data collected over 15 years, we found a 13.4% decrease in the survival of male deer mice with antibodies to SNV compared to uninfected mice (both male and female). There was also an additive effect of breeding condition, with a 21.3% decrease in survival for infected mice in breeding condition compared to uninfected, non-breeding mice. The data identified that transmission was consistent with density-dependent transmission, implying that there may be a critical host density below which SNV cannot persist. The notion of a critical host density coupled with the previously overlooked disease-induced mortality reported here contribute to a better understanding of why SNV often goes extinct locally and only seems to persist at the metapopulation scale, and why human spillover is episodic and hard to predict.
AB - How pathogens affect their hosts is a key question in infectious disease ecology, and it can have important influences on the spread and persistence of the pathogen. Sin Nombre virus (SNV) is the etiological agent of hantavirus pulmonary syndrome (HPS) in humans. A better understanding of SNV in its reservoir host, the deer mouse, could lead to improved predictions of the circulation and persistence of the virus in the mouse reservoir, and could help identify the factors that lead to increased human risk of HPS. Using mark-recapture statistical modeling on longitudinal data collected over 15 years, we found a 13.4% decrease in the survival of male deer mice with antibodies to SNV compared to uninfected mice (both male and female). There was also an additive effect of breeding condition, with a 21.3% decrease in survival for infected mice in breeding condition compared to uninfected, non-breeding mice. The data identified that transmission was consistent with density-dependent transmission, implying that there may be a critical host density below which SNV cannot persist. The notion of a critical host density coupled with the previously overlooked disease-induced mortality reported here contribute to a better understanding of why SNV often goes extinct locally and only seems to persist at the metapopulation scale, and why human spillover is episodic and hard to predict.
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U2 - 10.1007/s00442-011-2219-2
DO - 10.1007/s00442-011-2219-2
M3 - Article
C2 - 22218940
AN - SCOPUS:84861197685
SN - 0029-8549
VL - 169
SP - 431
EP - 439
JO - Oecologia
JF - Oecologia
IS - 2
ER -