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Zika virus: An emergent neuropathological agent.
Ann Neurol 2016; 80(4):479-89AN

Abstract

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.

Authors+Show Affiliations

Department of Neuroscience, Center for Neurovirology, Comprehensive NeuroAIDS Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.Department of Neuroscience, Center for Neurovirology, Comprehensive NeuroAIDS Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.Division of Infectious Diseases, Department of Medicine, Anschutz Medical Campus, University of Colorado, Aurora, CO. Department of Neurology, Anschutz Medical Campus, University of Colorado, Aurora, CO.Division of Infectious Diseases, Department of Medicine, Anschutz Medical Campus, University of Colorado, Aurora, CO. Department of Neurology, Anschutz Medical Campus, University of Colorado, Aurora, CO. Department of Microbiology and Immunology, Anschutz Medical Campus, University of Colorado, Aurora, CO.Department of Neuroscience, Center for Neurovirology, Comprehensive NeuroAIDS Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA. kamel.khalili@temple.edu.

Pub Type(s)

Historical Article
Journal Article
Review

Language

eng

PubMed ID

27464346

Citation

White, Martyn K., et al. "Zika Virus: an Emergent Neuropathological Agent." Annals of Neurology, vol. 80, no. 4, 2016, pp. 479-89.
White MK, Wollebo HS, David Beckham J, et al. Zika virus: An emergent neuropathological agent. Ann Neurol. 2016;80(4):479-89.
White, M. K., Wollebo, H. S., David Beckham, J., Tyler, K. L., & Khalili, K. (2016). Zika virus: An emergent neuropathological agent. Annals of Neurology, 80(4), pp. 479-89. doi:10.1002/ana.24748.
White MK, et al. Zika Virus: an Emergent Neuropathological Agent. Ann Neurol. 2016;80(4):479-89. PubMed PMID: 27464346.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Zika virus: An emergent neuropathological agent. AU - White,Martyn K, AU - Wollebo,Hassen S, AU - David Beckham,J, AU - Tyler,Kenneth L, AU - Khalili,Kamel, Y1 - 2016/08/10/ PY - 2016/03/30/received PY - 2016/07/25/revised PY - 2016/07/25/accepted PY - 2016/7/28/entrez PY - 2016/7/28/pubmed PY - 2017/6/6/medline SP - 479 EP - 89 JF - Annals of neurology JO - Ann. Neurol. VL - 80 IS - 4 N2 - 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. SN - 1531-8249 UR - https://www.unboundmedicine.com/medline/citation/27464346/Zika_virus:_An_emergent_neuropathological_agent_ L2 - https://doi.org/10.1002/ana.24748 DB - PRIME DP - Unbound Medicine ER -