ReviewImmunological reviews1999
Viruses, host responses, and autoimmunity.
Review in Immunological reviews, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 117 citations in OpenAlex.
- Viral infection and thyroid disorders: a narrative review.Frontiers in microbiology · 2025Review
- Natural IgG against S-Protein and RBD of SARS-CoV-2 Do Not Bind and Hydrolyze DNA and Are Not Autoimmune.International journal of molecular sciences · 2022Article
- Nervous System Manifestations of Arboviral Infections.Current tropical medicine reports · 2022Review
- Emerging Roles of Coronavirus in Autoimmune Diseases.Archives of medical research · 2021Review
- Coronavirus-induced autoimmunity.Clinical immunology (Orlando, Fla.) · 2021Review
- Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021Review
- Age-Associated Changes in Estrogen Receptor Ratios Correlate with Increased Female Susceptibility to Coxsackievirus B3-Induced Myocarditis.Frontiers in immunology · 2017Review
- Article
- Interleukin-6 (IL-6) and IL-17 synergistically promote viral persistence by inhibiting cellular apoptosis and cytotoxic T cell function.Journal of virology · 2014Article
- Autoimmune hepatitis: new paradigms in the pathogenesis, diagnosis, and management.Hepatology international · 2010Article
- Autoimmunity in Coxsackievirus B3 induced myocarditis: role of estrogen in suppressing autoimmunity.Future virology · 2010Article
- Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies.Molecular immunology · 2010Article
- A mathematical design of vector vaccine against autoimmune disease.Journal of theoretical biology · 2009Article
- Toll-like receptors in multiple sclerosis.Current topics in microbiology and immunology · 2009Review
- Article
- Cellular and humoral autoimmunity directed at bile duct epithelia in murine biliary atresia.Hepatology (Baltimore, Md.) · 2006Article
- Toll-like receptors and IFN-alpha: partners in autoimmunity.The Journal of clinical investigation · 2006Article
- Human foamy virus bel1 sequence in patients with autoimmune rheumatic diseases.Clinical rheumatology · 2006Article
- Detection of cytotoxic CD13-specific autoantibodies in sera from patients with ulcerative colitis and Crohn's disease.Journal of autoimmunity · 2006Review
- Virus-mediated autoimmunity in Multiple Sclerosis.Journal of autoimmune diseases · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conceptually, the initiation of autoimmune disease can be described as a three-stage process involving both genetic and environmental influences. This process begins with the development of an autoimmune cellular repertoire, followed by activation of these autoreactive cells in response to a localized target and, finally, the immune system's failure to regulate these self-reactive constituents. Viruses have long been associated with inciting autoimmune disorders. Two mechanisms have been proposed to explain how a viral infection can overcome immunological tolerance to self-components and initiate an organ-specific autoreactive process; these mechanisms are molecular mimicry and bystander activation. Both pathways, as discussed here, could play pivotal roles in the development of autoimmunity without necessarily excluding each other. Transgene technology has allowed us and others to examine more closely the roles of these mechanisms in mice and to dissect the requirements for initiating disease. These results demonstrate that bystander activation is the most likely explanation for disease development. Additional evidence suggests a further role for viruses in the reactivation and chronicity of autoimmune diseases. In this scenario, a second invasion by a previously infecting virus may restimulate already existing autoreactive lymphocytes, and thereby contribute to the diversity of the immune response.
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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.