This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mosquito-transmitted dengue virus, the agent of dengue fever, poses the most significant threat to public health of any arthropod-borne virus. Dengue viruses circulate in two distinct life cycles: (i) a global endemic cycle between humans and peridomestic Aedes mosquitoes, and (ii) a sylvatic cycle in the forests of West Africa and southeast Asia between arboreal Aedes mosquitoes and non-human primates. Endemic and sylvatic viruses show high genetic similarity, but sylvatic viruses do not cause outbreaks in humans. Our research has focused on identifying the barriers that limit the emergence of sylvatic dengue viruses. This is particularly important because if an effective dengue vaccine were developed, such barriers could come down. The current study tested the hypothesis that competition from established endemic strains could prevent sylvatic viruses from infecting peridomestic vector. We infected groups of Aedes aegypti, the major peridomestic vector, with one of 6 target virus strains: 3 strains of endemic dengue (serotype 2) and 3 strains of sylvatic dengue (serotype 2). Moreover each target strain was used in one of two treatments: single infection or mixed, concurrent infection with a common competitor (dengue serotype 4). We found that replication of each of the six target strains was unaffected by competition, since target virus concentration in the single-strain infections was not different from that of the mixed-strain infections. Future research will focus on the outcome of competition when the introduction of competitors is staggered in time.
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