Abstract
Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study. To determine whether responses to infection vary among geographic populations, we inoculated 3 populations of cotton rats with 2 enzootic VEEV strains (Co97-0054 [enzootic ID subtype] and 68U201 [enzootic IE subtype]). The 3 populations were offspring from wild-caught cotton rats collected in a VEE-enzootic area of south Florida, USA; wild-caught cotton rats from a non-VEE-enzootic area of Texas, USA; and commercially available (Harlan) colony-reared cotton rats from a non-VEE-enzootic region. Although each population had similar early viremia titers, no detectable disease developed in the VEE-sympatric Florida animals, but severe disease and death affected the Texas and Harlan animals. Our findings suggest that the geographic origins of cotton rats are important determinants of the outcome of VEE infection and reservoir potential of these rodents.
Highlights
Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study
To determine whether responses to infection vary among these geographic populations, we studied infection with 2 different subtypes of enzootic VEEV in 3 populations of cotton rats
Because some but not all North American populations occur in regions enzootic for VEE complex alphaviruses (e.g., Everglades virus (EVEV) in Florida), we attempted to better understand the host-VEEV interactions by inoculating 3 different populations with enzootic VEEV strains
Summary
Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study. Enzootic strains (subtype I, varieties D and E, as well as related species in the VEE complex comprising subtypes II–VI) have been regularly isolated in lowland tropical forests and swamps in Florida, Mexico, and Central and South America. These enzootic viruses generally circulate between Culex (Melanoconion) spp. mosquito vectors and rodent reservoirs and are usually avirulent for and incapable of amplification in equids [8]. Another study that examined clinical and histopathologic manifestations after infection of rats with Everglades virus (EVEV; subtype II in the VEE complex) reported that viremia developed and the virus replicated in a wide variety of organs, only 2% died [25]
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