In the case of DENV, there is no evidence for rapid evolution and selection as in HIV, influenza or SARS viruses; for DENV, man-made ecologic disruption or increments in the number of mosquitoes or hosts are more important than evolution towards more virulent genotypes. There has yet to be evidence for the circulation of a recombinant DENV and those recombinant genomes described to date have been the product of enzymatic amplification techniques and are thus probably lab artifacts (Aaskov et al. 2007; Holmes and Twiddy 2003; Worobey et al. 1999) ; no one has isolated and fully characterized a recombinant DENV that is being transmitted in nature, causing disease. Although there is evidence for recombination in other, positive-strand viruses, specific steps in DENV replication might keep this event from occurring, although ample opportunities seem to exist in multiplyinfected humans and mosquitoes (Monath et al. 2005) . Also, there is no evidence for the epidemic transmission of the sylvatic genotype viruses from West Africa or Malaysia. These older, seemingly less-virulent viruses are transmitted mainly by canopy-dwelling mosquitoes to monkeys and they do not cause outbreaks in the human populations inhabiting those areas. The viruses isolated from dengue patients during outbreaks belong to genotypes imported from other continents (in the case of serotype 2, a genotype originating in the Indian subcontinent was introduced to Africa) (Rico-Hesse 2003) . Some researchers, with ample field experience in tropical areas, believe that these zoonotic cycles will eventually disappear, because of the constant reduction of natural forests; thus, these cycles have practically no importance as reservoirs of human dengue (Rodhain 1991) .