ArticleVirusdisease2022
Identification of novel lncRNA by reanalysis of RNA-seq data in Zika Virus Infected hiNPCs.
Article in Virusdisease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- LncRNAJournal of virology · 2025Article
- Non-coding RNAs in the viral host-pathogen interaction: molecular regulation and therapeutic potential.Frontiers in cellular and infection microbiology · 2025Review
- Identification and functional prediction of long non-coding RNAs related to oxidative stress in the jejunum of piglets.Animal bioscience · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Zika Virus (ZIKV) infection is a serious, public health concern with no vaccines or antiviral treatments. This study aims to identify the differentially expressed long non-coding RNAs (lncRNAs) in ZIKV infected human-induced neuroprogenitor cells (hiNPCs). Though lncRNA is well-known for its role in gene regulation, its role in ZIKV infection remains unclear. Thus, taking advantage of publicly available transcriptome data, BioProject PRJNA551246 was analysed. Performed the gene ontology and pathway analysis of differentially expressed lncRNAs were functionally interpreted based on the neighbouring protein-coding genes (100 kb upstream and downstream of each lncRNAs). The study revealed 19 novels and 237 differentially expressed lncRNAs in ZIKV infected hiNPCs. They are found to be significantly enriched in type I interferon signalling pathway, negative regulation of viral genome replication, defense response to the virus, pathways involved in Influenza A and Herpes simplex infection, tumor necrosis factor signalling pathway, and apoptosis. In ZIKV, associated microcephaly type I interferon act as potential modulating factors. Type-I interferon inhibits ZIKV replication in many human cell types. The results support future studies on understanding the structure and function of the novel lncRNAs and experimental approaches to determine the role of the lncRNAs in ZIKV induced infection. Supplementary Information: The online version contains supplementary material available at 10.1007/s13337-022-00771-1.
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Registered trials
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