Abstract
Zika virus (ZIKV) is a kind of flavivirus emerged in French Polynesia and Brazil, and has led to a worldwide public health concern since 2016. ZIKV infection causes various neurological conditions, which are associated with fetus brain development or peripheral and central nervous systems (PNS/CNS) functional problems. To date, no vaccine or any specific antiviral therapy against ZIKV infection are available. It urgently needs efforts to explore the underlying molecular mechanisms of ZIKV-induced neural pathogenesis. ZIKV favorably infects neural and glial cells specifically astrocytes, consequently dysregulating gene expression and pathways with impairment of process neural cells. In this study, we applied a model for ZIKV replication in mouse primary astrocytes (MPAs) and profiled temporal alterations in the host transcriptomes upon ZIKV infection. Among the RNA-sequencing data of 27,812 genes, we examined 710 genes were significantly differentially expressed by ZIKV, which lead to dysregulation of numerous functions including neurons development and migration, glial cells differentiation, myelinations, astrocytes projection, neurogenesis, and brain development, along with multiple pathways including Hippo signaling pathway, tight junction, PI3K-Akt signaling pathway, and focal adhesion. Furthermore, we confirmed the dysregulation of the selected genes in MPAs and human astroglioma U251 cells. We found that PTBP1, LIF, GHR, and PTBP3 were upregulated while EDNRB and MBP were downregulated upon ZIKV infection. The current study highlights the ZIKV-mediated potential genes associated with neurodevelopment or related diseases.
Highlights
Zika virus (ZIKV) belongs to the Flaviviridae family, Flavivirus genus, and is transmitted to humans through Aedes mosquitoes bite and sexual intercourse [1,2,3]
This study reveals a series of dysregulation of neuropathic genes mRNA and protein expression in mouse and human astrocytes upon ZIKV infection
This study evaluated the alteration of neuropathic genes mRNA and protein expression in mouse primary astrocytes (MPAs) and human astroglioma U251 cells upon ZIKV infection
Summary
Zika virus (ZIKV) belongs to the Flaviviridae family, Flavivirus genus, and is transmitted to humans through Aedes mosquitoes bite and sexual intercourse [1,2,3]. ZIKV was isolated in the Zika forest of Uganda in 1947 from a monkey and the anti-ZIKV neutralizing antibodies in human serum were first reported in 1952 [7]. The first link between neurological diseases and ZIKV infection was described in the French Polynesia during the ZIKV outbreak in 2013–2014 [8,9]. Different approaches have been made to reveal the underlying links of microcephaly and ZIKV infection during pregnancy [11,12]. ZIKV infection is responsible for other neurological and brain abnormalities [10,11,13,14,15]
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