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Lancet. 2016 Apr 9;387(10027):1587-90. doi: 10.1016/S0140-6736(16)00650-4. Epub 2016 Mar 4.

Teratogenic effects of the Zika virus and the role of the placenta.

Author information

1
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA; Department of Obstetrics and Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: adibij@pitt.edu.
2
Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA, USA; The Research Center Aggeu Magalhães (CPqAM)/Oswaldo Cruz Foundation (Fiocruz), Recife, Brazil.
3
Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Sciences Center, Houston, TX, USA.
4
Department of Obstetrics and Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, USA.

Abstract

The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.

PMID:
26952548
DOI:
10.1016/S0140-6736(16)00650-4
[Indexed for MEDLINE]

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