| Literature DB >> 33657175 |
Pei Xu1, Junling Gao1, Chao Shan2, Tiffany J Dunn1, Xuping Xie2, Hongjie Xia2, Jing Zou2, Beatriz H Thames3, Amulya Sajja3, Yongjia Yu4, Alexander N Freiberg5, Nikos Vasilakis5,6,7,8, Pei-Yong Shi2,6, Scott C Weaver3,6,7,8, Ping Wu1.
Abstract
Global Zika virus (ZIKV) outbreaks and their strong link to microcephaly have raised major public health concerns. ZIKV has been reported to affect the innate immune responses in neural stem/progenitor cells (NS/PCs). However, it is unclear how these immune factors affect neurogenesis. In this study, we used Asian-American lineage ZIKV strain PRVABC59 to infect primary human NS/PCs originally derived from fetal brains. We found that ZIKV overactivated key molecules in the innate immune pathways to impair neurogenesis in a cell stage-dependent manner. Inhibiting the overactivated innate immune responses ameliorated ZIKV-induced neurogenesis reduction. This study thus suggests that orchestrating the host innate immune responses in NS/PCs after ZIKV infection could be promising therapeutic approach to attenuate ZIKV-associated neuropathology.Entities:
Mesh：
Year: 2021 PMID： 33657175 PMCID： PMC7959377 DOI： 10.1371/journal.pntd.0009183
Source DB: PubMed Journal: PLoS Negl Trop Dis ISSN： 1935-2727