Open AccessRole of microglia in the dissemination of Zika virus from mother to fetal brain
Author(s) -
Pei Xu,
Chao Shan,
Tiffany J. Dunn,
Xuping Xie,
Hongjie Xia,
Junling Gao,
Javier Allende Labastida,
Jing Zou,
Paula Villarreal,
Caitlin R. Schlagal,
Yongjia Yu,
Gracie Vargas,
Shannan L. Rossi,
Nikolaos Vasilakis,
Pei Yong Shi,
Scott C. Weaver,
Ping Wu
Publication year - 2020
Publication title -
plos neglected tropical diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.99
H-Index - 135
eISSN - 1935-2735
pISSN - 1935-2727
DOI - 10.1371/journal.pntd.0008413
Subject(s) - zika virus , microcephaly , microglia , biology , fetus , embryonic stem cell , virology , progenitor cell , immunology , virus , pregnancy , stem cell , microbiology and biotechnology , genetics , inflammation , gene
Global Zika virus (ZIKV) outbreaks and their link to microcephaly have raised major public health concerns. However, the mechanism of maternal-fetal transmission remains largely unknown. In this study, we determined the role of yolk sac (YS) microglial progenitors in a mouse model of ZIKV vertical transmission. We found that embryonic (E) days 6.5-E8.5 were a critical window for ZIKV infection that resulted in fetal demise and microcephaly, and YS microglial progenitors were susceptible to ZIKV infection. Ablation of YS microglial progenitors significantly reduced the viral load in both the YS and the embryonic brain. Taken together, these results support the hypothesis that YS microglial progenitors serve as “Trojan horses,” contributing to ZIKV fetal brain dissemination and congenital brain defects.