Abstract
The current Zika virus (ZIKV) outbreak is associated with neurological malformations and disorders in neonates. Areas of increased incidence of malformations may overlap with dengue-hyperendemic areas. ZIKV infection is enhanced by antibodies against dengue virus (DENV) in cell culture and inbred mice. Sufficiently powered clinical studies or primate studies addressing the enhancement of fetal ZIKV infection after previous dengue infection are not available. The human placenta is susceptible to ZIKV in vitro, but it is unknown whether antibody-dependent enhancement of ZIKV infection occurs at the placental barrier. Here we studied ZIKV infection in placental tissue in the presence of DENV-immune sera. Explants from the amniochorionic membrane, the chorionic villi, and the maternal decidua were infected with ZIKV in the presence of DENV type 1-, 2-, or 4-immune sera, or controls. Presence of DENV antibodies of any type enhanced the percentage of successful infections of organ explants between 1.42- and 2.67-fold, and led to a faster replication as well as significantly increased virus production. No enhancement was seen with yellow fever or chikungunya virus control sera. Pre-existing DENV antibodies may pose an increased risk of trans-placental ZIKV transmission.
Highlights
Zika virus (ZIKV) belongs to the genus Flavivirus and is related to other important human pathogens such as dengue virus (DENV), yellow fever virus (YFV) and West Nile virus
At 1 dpi, ZIKV replication was only seen in villous explants and only if these were infected in the presence of anti-DENV serum irrespective of DENV serotype
Placental villus (a), maternal decidua (b), and amnion (c) explants were infected in triplicates with ZIKV (1.5 × 105 PFU/mL) with or without prior incubation with human sera that either contained antibodies against one of three different DENV serotypes as indicated, YFV or chikungunya virus (CHIKV), or a control serum
Summary
Zika virus (ZIKV) belongs to the genus Flavivirus (family: Flaviviridae) and is related to other important human pathogens such as dengue virus (DENV), yellow fever virus (YFV) and West Nile virus. A distinct ZIKV lineage was first detected in an outbreak in Yap island in 20071, and subsequently affected the population of French Polynesia in 20132. The lineage adapted to urban circulation in South East Asia before emergence in the Pacific region and is thought to have been introduced to Brazil around 2013 to 2014, from where it spread within the Americas[3,4]. In Brazil, the resulting ZIKV epidemic in a non-immune population correlated with a rise in adverse pregnancy outcomes, notably an increase in microcephaly and other congenital conditions, first noticed in 20155. Evidence for maternal–fetal transmission with cerebral malformations was obtained for the outbreak in French Polynesia[6]
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