n 2006, an outbreak of chi k un - gunya fever — an arthralgic disease caused by a mosquito- borne alphavirus — swept over a number of islands in the Indian Ocean (the Comoros, Mauritius, the Seychelles, Madagascar, May- otte, and Reunion). In Reunion, which has a population of 770,000, there were 265,000 clinical cases (an incidence of 34%), and the dis- ease was implicated in 237 deaths (about 1 per 1000 clinical cases); a recent report by Reunion health authorities indicated that the se- roprevalence was 35%, with very few asymptomatic cases. The ep- idemic had started with outbreaks in Kenya in 2004 and the Comoros early in 2005. More recently, it jumped to India, where there have been an estimated 1.3 million cas- es to date.1 When all is said and done, the global toll of chikun- gunya in 2006 could be close to 2 million, and the disease may well continue to spread this year. Sequence analysis of the virus genome revealed that this mas- sive outbreak was caused by a new variant.2 Such changes are common in viruses that have a positive-stranded RNA genome, because the RNA-dependent RNA polymerase has no proofreading activity. A mutation in the E1 en- velope gene (A226V) has received special attention, and some re- searchers have proposed that this mutation may have modified the virus's ability to infect mosquitoes or perhaps even the severity of the illness associated with human in- fection. The mutation was report- ed to have occurred sometime be- tween the spring and the fall of 2005 — thus it cannot be impli- cated in the early stages of the epidemic (the Kenyan and Como- rian outbreaks) but may be to blame for the adaptation to a new mosquito vector. In the Makonde language,