Interspecies transmission and chikungunya virus emergence

- CHIKV adaptation to new urban vector, A. albopictus, can facilitate epidemics.
- Epistatic mutations can constrain adaptation of some CHIKV lineages to A. albopictus.
- CHIKV strains circulating in the Americas are less likely to adapt to A. albopictus.
- The risk for establishment of an enzootic CHIKV cycle in the neotropics is uncertain.
- Growing herd immunity will likely modulate the CHIKV pandemic.

Chikungunya virus (CHIKV) causes severe, debilitating, often chronic arthralgia with high attack rates, resulting in severe morbidity and economic costs to affected communities. Since its first well-documented emergence in Asia in the 1950s, CHIKV has infected millions and, since 2007, has spread widely, probably via viremic travelers, to initiate urban transmission in Europe, the South Pacific, and the Americas. Some spread has been facilitated by adaptive envelope glycoprotein substitutions that enhance transmission by the new vector, Aedes albopictus. Although epistatic constraints may prevent the impact of these mutations in Asian strains now circulating in the Americas, as well as in African CHIKV strains imported into Brazil last year, these constraints could eventually be overcome over time to increase the transmission by A. albopictus in rural and temperate regions. Another major determinant of CHIKV endemic stability in the Americas will be its ability to spill back into an enzootic cycle involving sylvatic vectors and nonhuman primates, an opportunity exploited by yellow fever virus but apparently not by dengue viruses.