Sin Nombre hantavirus decreases survival of male deer mice

Angela D. Luis, Richard J. Douglass, Peter J. Hudson, James N. Mills, Ottar N. Bjørnstad

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


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.

Original languageEnglish
Pages (from-to)431-439
Number of pages9
Issue number2
StatePublished - Jun 2012


  • Critical host density
  • Disease-induced mortality
  • Hantavirus
  • Mark-capture-recapture
  • Peromyscus
  • Sin Nombre virus


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