D T Mourya and A C Mishra (July 15, p 186)1 have rightly addressed the issue of the current chikungunya outbreak in India caused by the absence of herd immunity in the affected population.
However, re-emergence of this disease across India could be due to reasons beyond herd immunity. Schuffenecker and colleagues have reported the emergence of a new genotype with an A226V mutation in the membrane fusion glycoprotein E1 during the recent outbreak in the Indian Ocean islands.2 A similar genetic change is thought to have caused Semliki Forest virus, a close relative of chikungunya virus, to lose its dependence on cholesterol. Since mosquitoes often lack cholesterol, the newly emergent E1-226V variant might have adapted and survived better in mosquito species, thereby making Aedes albopictus—a previously redundant species in the chikungunya transmission cycle—the major vector in the present Reunion outbreak.3
In tropical and subtropical countries, enhanced transmission of arboviruses by mosquito vectors concurrently infected with microfilaria has been proved experimentally.4 Most of the reported cases of chikungunya (caused by an arbovirus) from the Indian subcontinent belong to coastal belts, which are endemic for filarial infections of variable severity. Thus, whether filarial parasitic infections are modulating the re-emergence of chikungunya deserves further investigation.