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2016 ; 80
(4
): 479-89
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Zika virus: An emergent neuropathological agent
#MMPMID27464346
White MK
; Wollebo HS
; David Beckham J
; Tyler KL
; Khalili K
Ann Neurol
2016[Oct]; 80
(4
): 479-89
PMID27464346
show ga
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.
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