ArticleNature communications2025
Single-cell eQTL mapping of human endogenous retroviruses reveals cell type-specific genetic regulation in autoimmune diseases.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- HERV2365 upregulates FGF1 expression by sponging miR-326 to promote the progression of intrahepatic cholangiocarcinoma.iScience · 2026Article
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
- Bioinformatics frameworks for single-cell long-read sequencing: unlocking isoform-level resolution.Briefings in bioinformatics · 2025Review
- Article
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Authors and funding
8 authors.
Funding
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Abstract
Human endogenous retroviruses constitute a significant portion of the human genome and play complex roles in gene regulation and disease processes. However, the expression pattern and disease associations of specific retroviral loci remain pooly understood. This study examines the expression and regulatory mechanisms of these retroviral elements in immune cells. Utilizing single-cell RNA sequencing data from peripheral blood mononuclear cells, we identify 41,460 expressed retroviral loci, with 1936 showing cell type-specific expression. We further detect 3463 conditionally independent expression quantitative trait loci linked to retroviral elements, highlighting their potential role in mediating genetic variants and disease associations. Notably, these retroviral sequences associate significantly with autoimmune diseases, with specific loci demonstrating pleiotropic associations with disease-related genes. Our findings suggest that these elements are not merely genomic remnants but active participants in cellular regulation and disease progression. This work advances understanding of human-retroviral coevolution and highlights potential therapeutic targets in immune disorders.
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