Most arboviruses are maintained in wild animal populations and only occasionally infect people. However, dengue (DEN) virus is an important exception that relies only on a human vertebrate reservoir and Aedes aegypti or Ae. albopictus mosquito vectors. Recent studies of DEN strains isolated from non-human primates or sylvan Aedes mosquitoes in Africa and Malaysia indicate that human DEN probably evolved from a sylvatic or jungle virus, and that epidemic DEN emergence occurred independently at least 4 times. We hypothesize that human urbanization and the concomitant peridomestication of Ae. aegypti and Ae. albopictus mosquitoes led to the emergence of DEN as an important urban disease in tropical countries. Urbanization of additional arboviruses and the emergence of other arboviral diseases will probably continue as tropical urban human populations expand and as Ae. albopictus and Ae. aegypti infest and reinfest these areas. This project will examine retrospectively the adaptation of DEN viruses to Ae. aegypti and Ae. albopictus peridomestic vectors. Our hypotheses is that epidemic dengue resulted from the adaptation of sylvatic progenitor dengue viruses to Ae. albopictus and Ae. aegypti mosquitoes. Evidence for viral adaptation will be sought using experimental infections; epidemic and sylvatic African vectors will be tested for their susceptibility and ability or transmit epidemic vs. sylvatic strains of dengue-2 virus strains from West Africa and elsewhere. The hypothesis predicts that sylvatic DEN viruses from Africa, representing an ancestral form, are more efficient at infecting sylvatic vectors than the derived, epidemic DEN strains. Conversely, the adapted epidemic strains should be capable of more efficient infection of and transmission by urban vectors than the sylvatic viruses. If the hypothesis is supported, these studies will form the basis for an expanded project to evaluate the genetic determinants of DEN virus adaptation to peridomestic vectors using infectious cDNA clones.
