The emergence of Zika virus in the Americas has followed a pattern that is 
familiar from earlier epidemics of other viruses, where a new disease is 
introduced into a human population and then spreads rapidly with important 
public health consequences. In the case of Zika virus, an accumulating body of 
recent evidence implicates the virus in the etiology of serious pathologies of 
the human nervous system, that is, the occurrence of microcephaly in neonates 
and Guillain-Barré syndrome in adults. Zika virus is an arbovirus 
(arthropod-borne virus) and a member of the family Flaviviridae, genus 
Flavivirus. Zika virions are enveloped and icosahedral, and contain a 
nonsegmented, single-stranded, positive-sense RNA genome, which encodes 3 
structural and 7 nonstructural proteins that are expressed as a single 
polyprotein that undergoes cleavage. Zika genomic RNA replicates in the 
cytoplasm of infected host cells. Zika virus was first detected in 1947 in the 
blood of a febrile monkey in Uganda's Zika Forest and in crushed suspensions of 
the Aedes mosquito, which is one of the vectors for Zika virus. The virus 
remained obscure, with a few human cases confined to Africa and Asia. There are 
two lineages of the Zika virus, African and Asian, with the Asian strain causing 
outbreaks in Micronesia in 2007 and French Polynesia in 2013-2014. From here, 
the virus spread to Brazil with the first report of autochthonous Zika 
transmission in the Americas in March 2015. The rapid advance of the virus in 
the Americas and its likely association with microcephaly and Guillain-Barré 
syndrome make Zika an urgent public health concern. Ann Neurol 2016;80:479-489.