A genetically distinct hantavirus, designated Oxbow virus (OXBV), was detected in tissues of an American shrew mole (Neurotrichus gibbsii), captured in Gresham, Oregon, in September 2003. Pairwise analysis of full-length S- and M- and partial L-segment nucleotide and amino acid sequences of OXBV indicated low sequence similarity with rodent-borne hantaviruses. Phylogenetic analyses using maximum-likelihood and Bayesian methods, and host-parasite evolutionary comparisons, showed that OXBV and Asama virus, a hantavirus recently identified from the Japanese shrew mole (Urotrichus talpoides), were related to soricine shrew-borne hantaviruses from North America and Eurasia, respectively, suggesting parallel evolution associated with cross-species transmission.

Prevalence of infection was highest where fewer animal species carried the virus.

Viruses in 6 genetic groups have caused recent outbreaks in Asia.

Hantavirus is a genus of virus represented by 45 different species and is hosted by small mammals, predominantly rats and mice. Roughly, half of all hantaviruses cause diseases in humans that vary in morbidity from mild to severe. The natural and anthropogenic changes occurring in the environment appear to be impacting the ecology of hantaviruses and their natural hosts as well as the incidence of hantaviral diseases in humans. Although such studies are limited at this time, there is evidence that natural climate cycles such as El Niño as well as anthropogenic climate change enhance hantavirus prevalence when host population dynamics are driven by food availability. Climate appears to have less of an effect on hantavirus when host populations are controlled by predators. Human alteration to the landscape also appears to enhance hantavirus prevalence when the disturbance regime enriches the environment for the host, for example, agriculture. More long-term studies on multiple species of hantavirus are needed to accurately predict the outcome of changing environmental conditions on prevalence in hosts as well as disease incidence in humans.

Animals infected with pathogens often differ in behaviour from their uninfected counterparts, and these differences may be key to understanding zoonotic pathogen transmission. To explore behavioural heterogeneity and its role in pathogen transmission, we studied deer mice, Peromyscus maniculatus, under field conditions. Deer mice are the natural host of Sin Nombre virus (SNV), a zoonotic pathogen with high human mortality. We live-trapped mice in May, July and September of 2009 and 2010, marked captures with passive integrated transponder (PIT) tags, recorded physical characteristics and collected blood samples for SNV analysis. For 4 nights after each trapping session, we observed behaviour with a novel surveillance system of nine camera stations, each consisting of a foraging tray, infrared camera, PIT antenna and data logger. We found that deer mice infected with SNV (30.0%) engaged more frequently in behaviours that increased the probability of intraspecific encounters and SNV transmission than did uninfected deer mice. When deer mice were categorized as bold (31.7%) or shy (68.3%) based on these behaviours, bold behaviour was predictive of positive SNV status. Bold deer mice were three times more likely to be infected with SNV than were shy deer mice. These results suggest that a small percentage of bold individuals are responsible for a majority of SNV transmission events, and that behavioural phenotype is an important consideration in transmission dynamics of zoonotic diseases.