Chikungunya Virus and Zika Virus in Europe

Chikungunya fever epidemics display secular, cyclical, and seasonal trends. These epidemics are characterized by explosive outbreaks inter- spersed by periods of disappearance ranging from several years to a few decades. Several mechanisms play a role: the human and the mosquito vector susceptibility to the virus; conditions facilitating mosquito breed- ing (resulting in a high vector density), ability of the vector to efficiently transmit the virus. There are historical accounts of epidemics of fever, arthralgias/arthritis, and rash, resembling what is now called “Chikungunya fever” dating back to 1824 from India and elsewhere (Kaur et al., 2008). Chikungunya virus (CHIKV) was firstly detected in Central/East Africa, where it is maintained in a sylvatic transmission cycle between nonhuman primates, small mammals (e.g., bats and monkeys) and Aedes mosquitoes . Urban chikungunya fever outbreaks are initiated by spillover infection of humans from enzootic African transmission cycles. The first identified outbreak of Chikungunya was reported from July 1952 to March 1953 in Tanzania. Since its discovery, numerous Chikungunya re-emergences have been documented. Currently, the Chikungunya virus has been identified in over 60 countries. The risk of importation of CHIKV into new areas is ever present because of the high attack rates associated with the recurring epidemics, the high levels of vi- remia in infected humans, and the worldwide distribution of the vectors responsible for transmitting CHIKV. E1-A226V and E2-L210Q mutations have been found to cause a dramatic increase in the infectivity of CHIKV, and the transmission of CHIKV has spread to Europe and the Americas because of the widespread distribution of the vectors Aedes aegypti and Ae. albopictus