ArticlePloS one2017
Genetic factors affecting EBV copy number in lymphoblastoid cell lines derived from the 1000 Genome Project samples.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 29 citations in OpenAlex.
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- Arginine Metabolism SupportsbioRxiv : the preprint server for biology · 2025Article
- Population-scale sequencing resolves correlates and determinants of latent Epstein-Barr Virus infection.bioRxiv : the preprint server for biology · 2025Article
- Landscape of the Epstein-Barr virus-host chromatin interactome and gene regulation.The EMBO journal · 2025Article
- Multiple sclerosis patient-derived spontaneous B cells have distinct EBV and host gene expression profiles in active disease.Nature microbiology · 2024Article
- The landscape of somatic mutations in lymphoblastoid cell lines.Cell genomics · 2023Article
- A high-throughput real-time PCR tissue-of-origin test to distinguish blood from lymphoblastoid cell line DNA for (epi)genomic studies.Scientific reports · 2022Article
- Mono a Mano: ZBP1's Love-Hate Relationship with the Kissing Virus.International journal of molecular sciences · 2022Review
- The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity.Nature communications · 2022Article
- Differentially Infiltrated Identification of Novel Diagnostic Biomarkers Associated with Immune Infiltration in Nasopharyngeal Carcinoma.Disease markers · 2022Article
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- Identifying genetic modulators of statin response using subject-derived lymphoblastoid cell lines.Pharmacogenomics · 2021Review
- Genetic variants in NKG2D axis and susceptibility to Epstein-Barr virus-induced nasopharyngeal carcinoma.Journal of cancer research and clinical oncology · 2021Article
- Gender and the Sex Hormone Estradiol Affect Multiple Sclerosis Risk Gene Expression in Epstein-Barr Virus-Infected B Cells.Frontiers in immunology · 2021Article
- The interaction of Multiple Sclerosis risk loci with Epstein-Barr virus phenotypes implicates the virus in pathogenesis.Scientific reports · 2020Article
- A reliable Epstein-Barr Virus classification based on phylogenomic and population analyses.Scientific reports · 2019Article
- An Atlas of Genetic Variation Linking Pathogen-Induced Cellular Traits to Human Disease.Cell host & microbe · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV), human herpes virus 4, has been classically associated with infectious mononucleosis, multiple sclerosis and several types of cancers. Many of these diseases show marked geographical differences in prevalence, which points to underlying genetic and/or environmental factors. Those factors may include a different susceptibility to EBV infection and viral copy number among human populations. Since EBV is commonly used to transform B-cells into lymphoblastoid cell lines (LCLs) we hypothesize that differences in EBV copy number among individual LCLs may reflect differential susceptibility to EBV infection. To test this hypothesis, we retrieved whole-genome sequenced EBV-mapping reads from 1,753 LCL samples derived from 19 populations worldwide that were sequenced within the context of the 1000 Genomes Project. An in silico methodology was developed to estimate the number of EBV copy number in LCLs and validated these estimations by real-time PCR. After experimentally confirming that EBV relative copy number remains stable over cell passages, we performed a genome wide association analysis (GWAS) to try detecting genetic variants of the host that may be associated with EBV copy number. Our GWAS has yielded several genomic regions suggestively associated with the number of EBV genomes per cell in LCLs, unraveling promising candidate genes such as CAND1, a known inhibitor of EBV replication. While this GWAS does not unequivocally establish the degree to which genetic makeup of individuals determine viral levels within their derived LCLs, for which a larger sample size will be needed, it potentially highlighted human genes affecting EBV-related processes, which constitute interesting candidates to follow up in the context of EBV related pathologies.
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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.