Microcephaly and Zika virus.

a a i o c w n c f t P s i s t t c e The original isolation of the Zika virus (ZIKV), a Flavivirus member of the Flaviviridae family, was obtained in 1947 from the blood of a febrile rhesus monkey exposed at the Zika forest near Lake Victoria, in the outskirts of Entebbe, the capital of Uganda.1 ZIKV was also isolated from wild mosquitoes in the same area and later periodic human febrile cases were attributed to ZIKV in Uganda and other countries in West and East Africa. Later, in the 1960s, ZIKV was detected in Asia and the virus was isolated from Aedes aegypti mosquitoes, initially in Malaysia and, subsequently, in several countries in Asia, showing that this arbovirus also occurred outside the African continent.2 This new facet of ZIKV, i.e., ability to cause epidemic disease transmitted by Aedes aegypti, disclosed a new milestone in the epidemiology of this arbovirus infection. It was clear that ZIKV had managed to adapt to an old acquaintance of humans, Aedes aegypti mosquitoes, transmitters of urban yellow fever, four serotypes of dengue fever, chikungunya virus, and other arboviruses in Asia and Africa. Since the 1960s, sporadic cases of ZIKV infection have been reported in humans3; due to its sporadic occurrence