| Literature DB >> 27247001 |
Kendra M Quicke1, James R Bowen1, Erica L Johnson2, Circe E McDonald1, Huailiang Ma3, Justin T O'Neal1, Augustine Rajakumar4, Jens Wrammert1, Bassam H Rimawi4, Bali Pulendran3, Raymond F Schinazi5, Rana Chakraborty2, Mehul S Suthar6.
Abstract
The recent Zika virus (ZIKV) outbreak in Brazil has been directly linked to increased cases of microcephaly in newborns. Current evidence indicates that ZIKV is transmitted vertically from mother to fetus. However, the mechanism of intrauterine transmission and the cell types involved remain unknown. We demonstrate that the contemporary ZIKV strain PRVABC59 (PR 2015) infects and replicates in primary human placental macrophages, called Hofbauer cells, and to a lesser extent in cytotrophoblasts, isolated from villous tissue of full-term placentae. Viral replication coincides with induction of type I interferon (IFN), pro-inflammatory cytokines, and antiviral gene expression, but with minimal cell death. Our results suggest a mechanism for intrauterine transmission in which ZIKV gains access to the fetal compartment by directly infecting placental cells and disrupting the placental barrier.Entities:
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Year: 2016 PMID： 27247001 PMCID： PMC5166429 DOI： 10.1016/j.chom.2016.05.015
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023