ArticleFrontiers in immunology2022
A High Prevalence of Anti-EBNA1 Heteroantibodies in Systemic Lupus Erythematosus (SLE) Supports Anti-EBNA1 as an Origin for SLE Autoantibodies.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 36 citations in OpenAlex.
- Viral metagenomic analysis of the blood virome in patients with multiple autoimmune diseases.Virology journal · 2026Article
- Impact of oncogenic viruses on autoimmune diseases and tumorigenesis.Infectious agents and cancer · 2026Review
- Multiple molecular mimics in Epstein Barr Nuclear Antigen-1, and the pathogenesis of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Epstein Barr virus antigen-induced autoantibodies against complement C1q exacerbate renal disease in lupus-prone mice.Frontiers in immunology · 2026Article
- Polygenic risk score and phenome-wide association study of the Epstein-Barr virus antibody response.Frontiers in genetics · 2026Article
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- Epstein-Barr virus reprograms autoreactive B cells as antigen-presenting cells in systemic lupus erythematosus.Science translational medicine · 2025Article
- A deep learning model for predicting systemic lupus erythematosus-associated epitopes.BMC medical informatics and decision making · 2025Article
- The Role of Epstein-Barr Virus in the Pathogenesis of Autoimmune Diseases.Medicina (Kaunas, Lithuania) · 2025Review
- Impact of Antibody Immune Response and Immune Cells on Osteoporosis and Fractures.Clinics in orthopedic surgery · 2025Article
- Antibody reactivity against EBNA1 and GlialCAM differentiates multiple sclerosis patients from healthy controls.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The toll like receptor 7 pathway and the sex bias of systemic lupus erythematosus.Frontiers in immunology · 2025Article
- Unlocking therapeutic potential: Targeting lymphocyte activation Gene-3 (LAG-3) with fibrinogen-like protein 1 (FGL1) in systemic lupus erythematosus.Journal of translational autoimmunity · 2024Review
- Epstein-Barr virus as a potentiator of autoimmune diseases.Nature reviews. Rheumatology · 2024Review
- Gene profiling of Epstein-Barr Virus and human endogenous retrovirus in peripheral blood mononuclear cells of SLE patients: immune response implications.Scientific reports · 2024Article
- The 330 risk loci known for systemic lupus erythematosus (SLE): a review.Frontiers in lupus · 2024Article
- Autologous Epstein-Barr virus-specific adoptive T-cell therapy in a patient with lupus nephritis.Clinical & translational immunology · 2024Article
- Shared Pathogenicity Features and Sequences between EBV, SARS-CoV-2, and HLA Class I Molecule-binding Motifs with a Potential Role in Autoimmunity.Clinical reviews in allergy & immunology · 2023Review
- Epstein-Barr virus infection as potential indicator of the occurrence and clinical presentation of systemic lupus erythematosus.Frontiers in immunology · 2023Article
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundThat Epstein-Barr virus (EBV) infection is associated with systemic lupus erythematosus (SLE) is established. The challenge is to explain mechanistic roles EBV has in SLE pathogenesis. Previous studies identify four examples of autoantibody cross-reactions between SLE autoantigens and Epstein-Barr nuclear antigen 1 (EBNA1). For two of these examples, the earliest detected autoantibody specifically cross-reacts with EBNA1; thereby, defined EBNA1 epitopes induce a robust autoantibody response in animals. These results suggest that the autoantibodies initiating the process leading to SLE may emerge from the anti-EBNA1 heteroimmune response. If this hypothesis is true, then anti-EBNA1 responses would be more frequent in EBV-infected SLE patients than in EBV-infected controls. We tested this prediction.
methodsWe evaluated published East Asian data by selecting those with a positive anti-viral capsid antigen (VCA) antibody immunoglobulin G (IgG) test and determining whether anti-EBNA1 was more common among the EBV-infected SLE cases than among matched EBV-infected controls with conditional logistic regression analysis.
resultsAll the qualifying SLE patients (100%) in this dataset were EBV-infected compared to age- and sex-matched controls (92.2%) [odds ratio (OR) = 28.6, 95% CI 6.4-∞, p = 8.83 × 10
conclusionsThe association of EBV infection with SLE is reconfirmed. The prediction that anti-EBNA1 is more frequent in these SLE cases than in EBV-infected controls is true, consistent with the hypothesis that anti-EBNA1 contributes to SLE. This second EBV-dependent risk factor is consistent with a molecular mimicry model for the generation of SLE, starting with EBV infection, progressing to anti-EBNA1 response; then molecular mimicry leads to anti-EBNA1 antibodies cross-reacting with an SLE autoantigen, causing autoantibody epitope spreading, and culminating in clinical SLE. These results support the anti-EBNA1 heteroimmune response being a foundation from which pathogenic SLE autoimmunity emerges.
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