Zika Virus Targets Different Primary Human Placental Cells, Suggesting Two Routes for Vertical Transmission
Takako Tabataa, Matthew Petitta, Henry Nelson Puerta-Guardob, Daniela Michlmayrb, Chunling Wangb, June Fang-Hoovera, Eva Harrisb c✉, Lenore Pereiraa d✉
- aDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, CA 94143, USA
- bDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley, Berkeley, CA 94720-3370, USA
- cDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley, Berkeley, CA 94720-3370, USA. Electronic address: eharris@berkeley.edu
- dDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: lenore.pereira@ucsf.edu
- ✉Corresponding author
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Abstract
Zika virus (ZIKV) infection during pregnancy is linked to severe birth defects, but mother-to-fetus transmission routes are unknown. We infected different primary cell types from mid- and late-gestation placentas and explants from first-trimester chorionic villi with the prototype Ugandan and a recently-isolated Nicaraguan ZIKV strain. ZIKV infects primary human placental cells and explants – cytotrophoblasts, endothelial cells, fibroblasts and Hofbauer cells in chorionic villi and amniotic epithelial cells, and trophoblast progenitors in amniochorionic membranes expressing Axl, Tyro3 and/or TIM1 viral entry cofactors. ZIKV produced NS3 and E proteins and generated higher viral titers in amniotic epithelial cells from mid-gestation compared to late-gestation placentas. Duramycin, a peptide that binds phosphatidylethanolamine in enveloped virions and precludes TIM1 binding, reduced ZIKV infection in placental cells and explants. Our results suggest that ZIKV spreads from basal and parietal decidua to chorionic villi and amniochorionic membranes, and targeting TIM1 could suppress infection at the uterine-placental interface.
TL;DRIt is suggested that ZIKV spreads from basal and parietal decidua to chorionic villi and amniochorionic membranes, and targeting TIM1 could suppress infection at the uterine-placental interface, and targeting TIM1 could suppress infection at the uterine-placental interface. (Semantic Scholar)