Abstract
In the summer of 2007, an unexpected outbreak of chikungunya (CHIK) fever, an arbovirus belonging to the Alphavirus genus, caused more than 200 human cases in the Emilia-Romagna Region of Italy; most of the cases were recorded in two villages in the Province of Ravenna.1 The tropical virus—which since late 2004 has caused several outbreaks in coastal Kenya, in the Indian Ocean (especially on the island of La Reunion) and on the Indian subcontinent—was introduced in Italy by a man from Kerala (an Indian state affected by a large outbreak) and sustained by local mosquitoes (Aedes albopictus, ‘the tiger mosquito’), which transmitted the infection to other persons. The epidemic can be said to have been the result of the globalization of vectors and humans, which occurred through a two-step process: (i) the introduction and adaptation of A. albopictus to a new environment (i.e. an area with a temperate climate); and (ii) the introduction of chikungunya virus (CHIKV) in a previously infection-free country as a result of population movement. The CHIKV strains introduced in Italy contained a mutation in the E1 glycoprotein which was responsible for a single amino acid substitution (A226V) able to increase the infectivity of the virus for A. albopictus.2,3