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Until 2005, chikungunya virus (CHIKV) was a relatively littlestudied pathogen restricted to parts of Africa and Asia. Epidemics were sporadic and separated by years of quiescence. In late 2004, the East Central South African genotype of CHIKV moved from Kenya onto the Indian Ocean island of Comoros. The global onslaught of CHIKV had begun. In November of 2005, viral isolates were identified with, what might normally be regarded as an insignificant, single alanine to valine mutation at position 226 of the envelope E1 gene. 1 This simple mutation had a remarkable effect; making the virus approximately 100 times more infectious to the Asian tiger mosquito, Aedes albopictus, and it was this species that was transmitting the virus rather than the usual vector, Aedes aegypti. 2 Subsequent ‘second-step’ mutations further enhanced the ability of the virus to infect and/or disseminate from the midgut to the salivary glands in Ae. albopictus. 3 However, these viruses can still be transmitted byAe. aegypti. Within a yearof the Indian Ocean lineage emerging, over 250 000 people had been infected. An epidemic in Asia began within months and has infected several million people in India and other Asian countries. Chikungunya infectionsoccurred in manycountriesasaresult ofpeopletravelling fromareaswith activetransmission.The presence oftiger mosquito vector has been critical to enable localized CHIKVoutbreaks in Italy and France. This species continues to invade new territory, 4 being

Chikungunya: here today, where tomorrow?