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Virol J. 2017 Nov 7;14(1):217. doi: 10.1186/s12985-017-0882-6.

ZIKV infection effects changes in gene splicing, isoform composition and lncRNA expression in human neural progenitor cells.

Author information

1
Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Kunming, 650223, China.
2
Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, 650204, China.
3
State Key Laboratory of Virology, CAS Center for Excellence in Brain Science and Intelligence Technology (CEBSIT), Wuhan Institute of Virology, Wuhan, 430071, China.
4
BGI-Yunnan, BGI-Shenzhen, Kunming, 650000, China.
5
College of Life Sciences, Yunnan University, Kunming, 650091, China.
6
Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Kunming, 650223, China. zhoujm@mail.kiz.ac.cn.

Abstract

BACKGROUND:

The Zika virus (ZIKV) is a mosquito-borne flavivirus that causes microcephaly and Guillain-Barré syndrome in infected individuals. To obtain insights into the mechanism of ZIKV infection and pathogenesis, we analyzed the transcriptome of ZIKV infected human neural progenitor cells (hNPCs) for changes in alternative splicing (AS), gene isoform (ISO) composition and long noncoding RNAs (lncRNAs) expression.

METHODS:

We analyzed differentially expressed lncRNAs, AS, ISO from RNA-seq data in ZIKV infected hNPCs.

RESULTS:

We obtained 149 differentially expressed lncRNAs, including potential viral targets to modulate cellular processes such as cell cycle, apoptosis and immune response. The infection induced 262 cases of AS occurring in 229 genes, which were enriched in cell death, RNA processing, transport, and neuron development. Among 691 differentially expressed ISOs, upregulated ISOs were enriched in signaling, regulation of transcription, and amino acid biosynthesis, while downregulated ISOs were mostly enriched in cell cycle. Importantly, these analyses revealed specific links between ZIKV induced changes in cellular pathways and the type of changes in the host transcriptome, suggesting important regulatory mechanisms.

CONCLUSIONS:

Our analyses revealed candidate lncRNAs, AS events and ISOs which may function in ZIKV infection induced cell cycle disruption, apoptosis and attenuation of neurogenesis, and shed light on the roles of lncRNAs, AS and ISOs in virus-host interactions, and would facilitate future studies of ZIKV infection and pathogenesis.

KEYWORDS:

Alternative splicing; Gene isoform; ZIKV; hNPC; lncRNA

PMID:
29116029
PMCID:
PMC5688814
DOI:
10.1186/s12985-017-0882-6
[Indexed for MEDLINE]
Free PMC Article

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