CHIKV belongs to the alphavirus genus of the Togaviridae family [12]. It belongs to the Semliki Forest virus antigenic complex that also contains the O’Nyong Nyong, Mayaro, and Ross River viruses. It is an enveloped positive-strand RNA virus, with a genome of about 12 kb. The genome is capped in 5′ and has a polyA tail in the 3′ end. It encodes four nonstructural proteins (nsP1 to nsP4) and five structural proteins (C-E3-E2-6 k-E1). Genetic analysis based on the E1 envelope glycoprotein sequences showed three distinct lineages: the West African cluster, the East-Central and South African cluster (ECSA), and the Asian cluster [13]. It is thought that CHIKV originated in West Africa, colonized other African areas, and was secondarily introduced into Asia before the 1960s [14••]. The viral situation remained stable for five decades. Strains circulating in the Western Indian Ocean in the 2000s were related to the ESCA lineage [12]. The most significant event in CHIKV history was the appearance of an adaptive mutation, an alanine-to-valine substitution at position 226 in the E1 glycoprotein gene (E1:A226V) on an ESCA-CHIKV strain circulating on Reunion Island after September 2005. It led the mutated CHIKV to lose cholesterol dependence for growth and enhanced its infectivity, replication, and transmission by Ae. albopictus, without impairing common vectorial capability of Ae. aegypti [15, 16]. Similar genetic events occurred independently in India, Gabon, and Cameroon, suggesting an evolutionary convergence of the virus to this mosquito and a great subsequent ability for worldwide epidemic expansion [13, 17, 18]. To date, no difference in virulence between the different strains of CHIKV has been shown in humans