Abstract
Sin Nombre hantavirus (SNV), hosted by the North American deermouse (Peromyscus maniculatus), causes hantavirus pulmonary syndrome (HPS) in North America. Most transmission studies in the host were conducted under artificial conditions, or extrapolated information from mark-recapture data. Previous studies using experimentally infected deermice were unable to demonstrate SNV transmission. We explored SNV transmission in outdoor enclosures using naturally infected deermice. Deermice acquiring SNV in enclosures had detectable viral RNA in blood throughout the acute phase of infection and acquired significantly more new wounds (indicating aggressive encounters) than uninfected deermice. Naturally-infected wild deermice had a highly variable antibody response to infection, and levels of viral RNA sustained in blood varied as much as 100-fold, even in individuals infected with identical strains of virus. Deermice that infected other susceptible individuals tended to have a higher viral RNA load than those that did not infect other deermice. Our study is a first step in exploring the transmission ecology of SNV infection in deermice and provides new knowledge about the factors contributing to the increase of the prevalence of a zoonotic pathogen in its reservoir host and to changes in the risk of HPS to human populations. The techniques pioneered in this study have implications for a wide range of zoonotic disease studies.
Highlights
Recognition that most emerging infectious diseases are zoonotic [1] has led to increased investigation of wildlife host-pathogen systems designed to characterize pathogens, identify hosts, and describe environmental factors associated with transmission, in order to develop predictive tools and inform control and prevention policies
We tested whether Sin Nombre hantavirus (SNV)-infected deermice were more likely to be wounded and accrue more wounds than uninfected mice
We demonstrated viral RNA in blood for at least 8 weeks PI
Summary
Recognition that most emerging infectious diseases are zoonotic [1] has led to increased investigation of wildlife host-pathogen systems designed to characterize pathogens, identify hosts, and describe environmental factors associated with transmission, in order to develop predictive tools and inform control and prevention policies. After a highly fatal outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern USA in 1993, an interdisciplinary team identified a novel hantavirus, Sin Nombre hantavirus (SNV), as the causative agent and the North American deermouse (Peromyscus maniculatus; hereafter referred to as ‘‘deermouse’’) as the host [2,3]. Field studies identified environmental conditions associated with increased deermouse populations and transmission in those populations, and described conditions favorable for human infection. These findings lead to predictive models [4,5], and successful interventions to mitigate human disease [6,7]. Numerous SNV-like viruses associated with various rodent hosts have been identified throughout the Americas [8,9]
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