Phylogenetic analysis of the viral sequences of our patients has revealed that the circulating strains were of the Indian Ocean genotype and closely related to those from the 2006 outbreak in India [29] but without the A226V mutation, further emphasizing how remarkably rapid the disease could spread with the right environmental conditions. The attack rate in our outbreak was 0.5%, much lower than the 34% reported in Reunion Island and the 5.4% observed in Italy [13, 30] . This could be attributed to the rapid removal of human reservoirs through isolation, enhanced vector control, or the circulation of a virus strain of lower epidemic potential. Clinical features of our patients were similar to those reported in recent outbreaks [6] [7] [8] [9] [11] [12] [13] [14] [16] [17] [18] 21, 30] , indicating that although people are genetically diverse response to diseases is homogeneous across people in non-homogeneous populations. The majority of our patients was #45 years and had no premorbid condition. Unlike patients reported in the Reunion Island outbreak [6] , where the patients' underlying medical conditions could have contributed to the observed morbidities, our patients were younger and healthier. Furthermore, none of our patients was co-infected with dengue, as confirmed by RT-PCR and dengue enzyme-linked immunoabsorbent assay (ELISA)-IgM and IgG [31] . Hence, our immunologic observations can be largely attributed to acute CHIKV infection itself.