• Kjersti M Aagaard, Anismrita Lahon, Melissa A Suter, Ravi P Arya, Maxim D Seferovic, Megan B Vogt, Min Hu, Fabio Stossi, Michael A Mancini, R Alan Harris, Maike Kahr, Catherine Eppes, Martha Rac, Michael A Belfort, Chun Shik Park, Daniel Lacorazza, and Rebecca Rico-Hesse.
• Departments of Obstetrics &Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine &Texas Children's Hospital, Houston, TX, USA.
• Sci Rep. 2017 Jan 27; 7: 41389.

AbstractZika virus (ZIKV) is an emerging mosquito-borne (Aedes genus) arbovirus of the Flaviviridae family. Although ZIKV has been predominately associated with a mild or asymptomatic dengue-like disease, its appearance in the Americas has been accompanied by a multi-fold increase in reported incidence of fetal microcephaly and brain malformations. The source and mode of vertical transmission from mother to fetus is presumptively transplacental, although a causal link explaining the interval delay between maternal symptoms and observed fetal malformations following infection has been missing. In this study, we show that primary human placental trophoblasts from non-exposed donors (n = 20) can be infected by primary passage ZIKV-FLR isolate, and uniquely allowed for ZIKV viral RNA replication when compared to dengue virus (DENV). Consistent with their being permissive for ZIKV infection, primary trophoblasts expressed multiple putative ZIKV cell entry receptors, and cellular function and differentiation were preserved. These findings suggest that ZIKV-FLR strain can replicate in human placental trophoblasts without host cell destruction, thereby serving as a likely permissive reservoir and portal of fetal transmission with risk of latent microcephaly and malformations.

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