期刊
EBIOMEDICINE
卷 10, 期 -, 页码 71-76出版社
ELSEVIER
DOI: 10.1016/j.ebiom.2016.07.018
关键词
-
资金
- Labex CelTisPhyBio [11-LBX-0038]
- Idex Paris Sciences et Lettres [ANR-10-IDEX-0001-02 PSL]
- Ministry of Defence/Direction Generale de l'Armement (DGA)
- European Research Council [339847]
- [278433-PREDEMICS]
- European Research Council (ERC) [339847] Funding Source: European Research Council (ERC)
The recent Zika outbreak in South America and French Polynesia was associated with an epidemic of microcephaly, a disease characterized by a reduced size of the cerebral cortex. Other members of the Flavivirus genus, including West Nile virus (WNV), can cause encephalitis but were not demonstrated to cause microcephaly. It remains unclear whether Zika virus (ZIKV) and other flaviviruses may infect different cell populations in the developing neocortex and lead to distinct developmental defects. Here, we describe an assay to infect mouse E15 embryonic brain slices with ZIKV, WNV and dengue virus serotype 4 (DENV-4). We show that this tissue is able to support viral replication of ZIKV and WNV, but not DENV-4. Cell fate analysis reveals a remarkable tropism of ZIKV infection for neural stem cells. Closely related WNV displays a very different tropism of infection, with a bias towards neurons. We further show that ZIKV infection, but not WNV infection, impairs cell cycle progression of neural stem cells. Both viruses inhibited apoptosis at early stages of infection. This work establishes a powerful comparative approach to identify ZIKV-specific alterations in the developing neocortex and reveals specific preferential infection of neural stem cells by ZIKV. (C) 2016 The Authors. Published by Elsevier B.V.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据