Abstract
Zika virus (ZIKV) infection is associated with microcephaly in fetuses, but the pathogenesis of ZIKV-related microcephaly is not well understood. Here we show that ZIKV infects the subventricular zone in human fetal brain tissues and that the tissue tropism broadens with the progression of gestation. Our research demonstrates also that intermediate progenitor cells (IPCs) are the main target cells for ZIKV. Post-mitotic committed neurons become susceptible to ZIKV infection as well at later stages of gestation. Furthermore, activation of microglial cells, DNA fragmentation, and apoptosis of infected or uninfected cells could be found in ZIKV-infected brain tissues. Our studies identify IPCs as the main target cells for ZIKV. They also suggest that immune activation after ZIKV infection may play an important role in the pathogenesis of ZIKV-related microcephaly.
Highlights
IntroductionA number of groups have addressed the question of which cell type might be targeted by using induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) as model systems
Zika virus (ZIKV) has been isolated from brain tissues of newborns with microcephaly[1]
In fetal brain tissues from the 15.5 GW donor, we observed that the subventricular zone was highly susceptible, whereas the intermediate zone and the cortical plate were less permissive to ZIKV infection
Summary
A number of groups have addressed the question of which cell type might be targeted by using induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) as model systems. Their studies have concluded that ZIKV infects neural progenitor cells derived from induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs)[32,33,34,35]. It impairs neurosphere survival and growth of iPSC/ESC-derived brain organoids[32,36]. To better understand the pathogenesis of ZIKV-related microcephaly, we investigated the tissue and cellular tropism of ZIKV in human fetal brain tissues
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