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Emergence of arboviruses could result from their ability to exploit new environments, for example a new host. This ability is facilitated by the high mutation rate occurring during viral genome replication. The last emergence of chikungunya in the Indian Ocean region corroborates this statement since a single viral mutation at the position 226 on the E1 glycoprotein (E1-A226V) was associated with enhanced transmission by the mosquito  Aedes albopictus  in regions where the major mosquito vector,  Aedes aegypti , is absent.  We used direct competition assays  in vivo  to dissect out the mechanisms underlying the selection of E1-226V by  Ae. albopictus . When the original variant E1-226A and the newly emerged E1-226V were provided in the same blood-meal at equal titers to both species of mosquitoes, we found that the proportion of both variants was drastically different in the two mosquito species. Following ingestion of the infectious blood-meal, the E1-226V variant was preferentially selected in  Ae. albopictus , whereas the E1-226A variant was sometimes favored in  Ae. aegypti . Interestingly, when the two variants were introduced into the mosquitoes by intrathoracic inoculations, E1-226V was no longer favored for dissemination and transmission in  Ae. albopictus , showing that the midgut barrier plays a key role in E1-226V selection.  This study sheds light on the role of the midgut barrier in the selection of novel arbovirus emerging variants. We also bring new insight into how the pre-existing variant E1-226V was selected among other viral variants including E1-226A. Indeed the E1-226V variant present at low levels in natural viral populations could rapidly emerge after being selected in  Ae. albopictus  at the midgut barrier level.

Dissemination and Transmission of the E1-226V Variant of Chikungunya Virus in Aedes albopictus Are Controlled at the Midgut Barrier Level