ArticleFrontiers in immunology2025
Study on the spatiotemporal regulation of interferon-stimulated genes during Zika virus infection.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Background: Zika virus (ZIKV) can cause severe neurological disorders such as congenital microcephaly, and there are currently no approved prevention or treatment measures. Elucidating the antiviral mechanism of the host interferon-stimulated genes (ISGs) is crucial for the development of therapeutic strategies. Methods: This study integrated multisystem transcriptomic data [human brain organoids, monocyte-derived dendritic cells (moDCs), and peripheral blood mononuclear cells (PBMCs) from infected patients], combined with cellular experiments and bioinformatics analysis, to systematically investigate the spatiotemporal regulation characteristics and functions of ISGs during ZIKV infection. Results: The results showed that treatment with interferon beta (IFN-β) significantly activated the ISGs (e.g., IRF7 and IFITM3) in the ZIKV-infected brain organoids, which were enriched in virus defense-related pathways. Single-cell transcriptomics revealed cellular heterogeneity in the IFN-β-driven ISG responses in moDCs. Transcriptomic analysis of the PBMCs identified 210 differentially expressed genes between the acute and convalescent phases. Core ISGs (e.g., RSAD2 and OAS3) were transiently upregulated in the acute phase. Through cross-analysis, 22 cross-system shared ISGs were screened out. Least absolute shrinkage and selection operator (LASSO) regression identified 11 potential diagnostic biomarkers for ZIKV infection. Small interfering RNA (siRNA) knockdown experiments confirmed that IFI35, IFI44, and OAS3 exerted antiviral effects by inhibiting ZIKV replication. Conclusion: This study reveals the functional plasticity of ISGs and provides key targets and theoretical support for the prevention and treatment of ZIKV.
Indexed as
Identifiers
What 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.