68 research outputs found

    Natural Enzootic Vectors of Venezuelan equine encephalitis virus in the Magdalena Valley, Colombia

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    To characterize the transmission cycle of enzootic Venezuelan equine encephalitis virus (VEEV) strains believed to represent an epizootic progenitor, we identified natural vectors in a sylvatic focus in the middle Magdalena Valley of Colombia. Hamster-baited traps were placed into an active forest focus, and mosquitoes collected from each trap in which a hamster became infected were sorted by species and assayed for virus. In 18 cases, a single, initial, high-titered mosquito pool representing the vector species was identified. These vectors included Culex (Melanoconion) vomerifer (11 transmission events), Cx. (Mel.) pedroi (5 transmissions) and Cx. (Mel.) adamesi (2 transmissions). These results extend the number of proven enzootic VEEV vectors to 7, all of which are members of the Spissipes section of the subgenus Melanoconion. Our findings contrast with previous studies, which have indicated that a single species usually serves as the principal enzootic VEEV vector at a given location

    Genetic and Anatomic Determinants of Enzootic Venezuelan Equine Encephalitis Virus Infection of Culex (Melanoconion) taeniopus

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    Venezuelan equine encephalitis (VEE) is a re-emerging, mosquito-borne viral disease with the potential to cause fatal encephalitis in both humans and equids. Recently, detection of endemic VEE caused by enzootic strains has escalated in Mexico, Peru, Bolivia, Colombia and Ecuador, emphasizing the importance of understanding the enzootic transmission cycle of the etiologic agent, VEE virus (VEEV). The majority of work examining the viral determinants of vector infection has been performed in the epizootic mosquito vector, Aedes (Ochlerotatus) taeniorhynchus. Based on the fundamental differences between the epizootic and enzootic cycles, we hypothesized that the virus-vector interaction of the enzootic cycle is fundamentally different from that of the epizootic model. We therefore examined the determinants for VEEV IE infection in the enzootic vector, Culex (Melanoconion) taeniopus, and determined the number and susceptibility of midgut epithelial cells initially infected and their distribution compared to the epizootic virus-vector interaction. Using chimeric viruses, we demonstrated that the determinants of infection for the enzootic vector are different than those observed for the epizootic vector. Similarly, we showed that, unlike A. taeniorhynchus infection with subtype IC VEEV, C. taeniopus does not have a limited subpopulation of midgut cells susceptible to subtype IE VEEV. These findings support the hypothesis that the enzootic VEEV relationship with C. taeniopus differs from the epizootic virus-vector interaction in that the determinants appear to be found in both the nonstructural and structural regions, and initial midgut infection is not limited to a small population of susceptible cells
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