ArticleVirus genes2025
Robust antiviral innate immune response and miRNA regulatory network were identified in ZIKV-infected cells: implications in the pathogenesis of ZIKV infection.
Article in Virus genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- MX1 is a novel crucial prognostic and therapeutic target inducing chemoresistance in right-sided colon cancer: insights from machine learning-based multi-omics analysis.Human genomics · 2025Article
- Non-coding RNAs in the viral host-pathogen interaction: molecular regulation and therapeutic potential.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Zika virus (ZIKV) infection has emerged as a significant public health concern due to its association with fetal microcephaly and Guillain-Barre syndrome (GBS). Unfortunately, its detailed pathogenesis remains unclear. To better understand how ZIKV evades host antiviral immunity, we analyzed the microarray dataset (GSE98889) of ZIKV-infected primary human brain microvascular endothelial cells (hBMECs) retrieved from the gene expression omnibus (GEO). 160, 1423, 969, 829, and 600 differentially expressed genes (DEGs) were identified at 12, 24, 48, 72, and 216 hours post-ZIKV infection in hBMECs, respectively. Subsequently, 31 common DEGs across all time-points were selected for further analysis. Gene ontology (GO) functional analysis showed these 31 DEGs were mainly involved in the host antiviral innate immune responses. Protein-protein interaction (PPI) network analysis identified 10 hub genes (MX1, OAS1, OAS2, IFI44, IFI44L, IFIT1, IFIT2, IFIT3, IFIH1, and XAF1), which were all interferon-stimulated genes (ISGs) and upregulated. qRT-PCR was used to validate the expression patterns of these 10 hub genes in different ZIKV-infected cell lines. Finally, miRNA-mRNA regulatory network analysis revealed that hsa-miR-129-2-3p, hsa-miR-138-5p, hsa-miR-21-3p, hsa-miR-27a-5p, hsa-miR-449a, and hsa-miR449b-5p were key miRNAs regulating these hub genes. Our study showed that ZIKV infection activated the host innate immune response to restrict ZIKV infection. The common pathways, hub genes, and their regulatory miRNA network offer new insights into virus-host interactions, enhancing our understanding of ZIKV pathogenesis.
Indexed as
Identifiers
39955676What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.