ReviewClinical & developmental immunology2012
Epstein-Barr virus and systemic lupus erythematosus.
Review in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 142 citations in OpenAlex.
- Divergent autoimmune genetic landscapes in diabetic and non-diabetic individuals.BMC genomic data · 2026Article
- Article
- Co-occurrence of viral encephalitis and autoimmune encephalitis: overlapping peaks encephalitis or coincidence condition?BMC neurology · 2026Article
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- Impact of oncogenic viruses on autoimmune diseases and tumorigenesis.Infectious agents and cancer · 2026Review
- How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- Population-scale sequencing resolves correlates and determinants of latent Epstein-Barr Virus infection.bioRxiv : the preprint server for biology · 2025Article
- Long Term Outcomes of Anti-COVID-19 Vaccines in Patients with Systemic Lupus Erythematosus: A Multicentre Study.Vaccines · 2025Article
- Human herpesvirus reactivation and its potential role in the pathogenesis of post-acute sequelae of SARS-CoV-2 infection.GeroScience · 2025Review
- Review
- How artificial intelligence can enable personalized mesenchymal stem cell-based therapeutic strategies in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Cancer in connective tissue disease.Frontiers in immunology · 2025Review
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Autoantibodies in COVID-19: implications for disease severity and clinical outcomes.Frontiers in immunology · 2024Review
- Autologous Epstein-Barr virus-specific adoptive T-cell therapy in a patient with lupus nephritis.Clinical & translational immunology · 2024Article
- Assessment of the humoral immune status of varicella-zoster virus in patients with diffuse connective tissue diseases.Frontiers in medicine · 2024Article
- An IL-17A-centric response to Epstein-Barr virus DNA mediated by dendritic Cell-T cell interactions.Frontiers in molecular biosciences · 2024Article
- Antibody Cross-Reactivity in Auto-Immune Diseases.International journal of molecular sciences · 2023Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens.
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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.