And epstein barr virus infection

Sinus inflammation. Increased spleen size. Do you have more information about symptoms of this disease? We want to hear from you. Cause Cause. This allows the symptoms of an EBV infection to persist and get worse over time.

Diagnosis Diagnosis. Treatment Treatment. Hematopoietic stem-cell transplant is currently the only curative treatment for this condition.

Statistics Statistics. Do you have updated information on this disease? Find a Specialist Find a Specialist. Healthcare Resources To find a medical professional who specializes in genetics, you can ask your doctor for a referral or you can search for one yourself. You can also learn more about genetic consultations from MedlinePlus Genetics. Research Research. Clinical Research Resources ClinicalTrials. Click on the link to go to ClinicalTrials. Please note: Studies listed on the ClinicalTrials.

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Have a question? References References. Characterization and treatment of chronic active Epstein-Barr virus disease: a year experience in the United States. June 2, ; 22 Infectious mononucleosis. The team found that a viral protein called EBNA2 was associated with nearly half of the genetic regions associated with the risk for lupus. EBNA2 is known to work through human transcription factors, which bind to DNA and affect the expression of genes nearby.

The team also used RELI to compare the genetic regions tied to risk of other autoimmune diseases. They found that EBNA2 bound to regions associated with the risk for multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis, and celiac disease. Many transcription factors were associated with these regions as well. Anthony S. References: Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity.

Nat Genet. PMID: Department of Veterans Affairs. The major clinical characteristics are xerostomia and xeropthalmia in addition to fatigue and various other symptoms, which may also affect other organ systems , The etiology of SS has been suggested to involve several environmental and genetic factors, molecular mimicry and bystander activation , Environmental factors include vitD deficiency, smoking, silica dust exposure and virus infections SLE is a disease, which clinically presents with a heterogenous array of symptoms, often evaluated by the SLE disease activity index SLEDAI or similar indexes, including complementemia, DNA Abs, leukopenia, thrombocytemia, fever, fatigue, skin rash, UV sensitivity, mucosal ulcers, alopecia, pleuriris or pericarditis, proteinuria, hematuria, nephritis, myositis, arthritis, vasculitis, headache, stroke, and more rarely, neuropsychiatric symptoms — SLE has been described as an immune complex disease, since it is often associated with decreased levels of complement components Genetically predisposing factors are first of all certain HLA-DRB1 alleles, but multiple immune system genes, including other MHC-II alleles and some MHC-I alleles, as well as genes affecting cellular waste removal, have been found to influence disease development , Major environmental factors promoting development of SLE are silica dust exposure, sun burn, smoking, vitD deficiency and EBV infection — Decreased immune control of chronic EBV infection has been found to be a contributing factor, if not a major cause , , , but other infections may also play a role in SLE development or exacerbation , These diseases share several genetic and environmental factors, in particular the predisposing effect of certain HLA-DRB1 alleles although not exactly identical alleles , the predisposing effect of EBV infection and of factors, which can be related to EBV infection e.

Current treatments can also be related to EBV infection, e. This results in production of EBV-transformed B cell blasts, which by their very nature will attempt homing to bones and therefore will have a tendency to populate joints, where the concomitant lytic EBV production may also result in EBV infection of synovial epithelial cells. In SLE, B cells will also be involved, thus accounting for the common involvement of joints and other symptoms overlapping with RA, however, the major target cells affected are epithelial cells, thus accounting for the common skin and mucosal pathology, while the defective removal of EBV and cellular debris results in immune complex deposition in affected organs and in particular kidneys, by virtue of their filtrating actions.

Other autoimmune diseases, especially MS have also been found to depend on EBV infection in several aspects The question therefore arises, how EBV can be involved in these apparently diverse diseases? A common feature seems to be decreased immune control of EBV. This allows for chronic infections with continuous cycles of relapses and remissions. However, while this may explain a common involvement of EBV or other viruses in disease etiology, it does not explain the different clinical appearances and the differences in e.

A plausible explanation is that the role of EBV does not depend solely on e. Other HLA interactions must also be involved, e. In general will the genetic composition of the host determine the fate of EBV in different cell types, including the interactions of EBV attachment and entry proteins with the target cell membrane proteins, the ability of the host cell to undergo apoptosis and the possibility to support lytic production of virus, and the efficiency of adaptive immune control of EBV.

Patients with SADs are often prone to various infections, possibly due to inherent or acquired immune deficiencies, which predispose to coinfection with other viruses e. Patients with SADs also have increased tendency to develop cancer, including various forms of lymphoma. This may relate to secondary effects of treatment with immuno-suppressive drugs but may also reflect an inherent ability of EBV to cause transformation of B cells and epithelial cells 13 , 99 — , It remains unclear, whether the role of EBV is primarily in initiation of disease e.

All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. We acknowledge the contributions of all students and collaborators, who have participated in our studies on SADs. National Center for Biotechnology Information , U. Front Immunol.

Published online Jan 7. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology. Received Jul 25; Accepted Nov The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract Epstein-Barr Virus EBV is an extremely successful human herpes virus, which infects essentially all human beings at some time during their life span. Keywords: antibodies, Epstein-Barr virus, connective tissue disease, systemic autoimmune diseases, human herpes virus.

Open in a separate window. Figure 1. Figure 3. Epstein-Barr Virus Immune Evasion As a part of the common evolutionary history of humans and EBV, the virus has evolved a multitude of immune evasion mechanisms, including wrapping itself in host cell-derived membranes envelopment and the ability to switch between latent and lytic life stages 50 , Figure 2. Epstein-Barr Virus Epidemiology A majority of children becomes infected with EBV early in life and seroconversion, the appearance of Abs to EBV peaks around 1—2 years of life, where the majority of infectious cases is non-complicated and may even go unnoticed.

Systemic Autoimmune Diseases SADs are a group of partly overlapping syndromes, also called connective tissue diseases, since they often are accompanied by inflammation of connective tissues. Table 2 Systemic autoimmune diseases SADs and their characteristics. Epstein-Barr Virus and Rheumatoid Arthritis The clinical characteristics of RA are swollen and painful joints, caused by synovial inflammation eventually resulting in exaggerated connective tissue deposition pannus formation and bone erosion, with resulting disability.

Epstein-Barr Virus and Systemic Lupus Erythematosus SLE is a disease, which clinically presents with a heterogenous array of symptoms, often evaluated by the SLE disease activity index SLEDAI or similar indexes, including complementemia, DNA Abs, leukopenia, thrombocytemia, fever, fatigue, skin rash, UV sensitivity, mucosal ulcers, alopecia, pleuriris or pericarditis, proteinuria, hematuria, nephritis, myositis, arthritis, vasculitis, headache, stroke, and more rarely, neuropsychiatric symptoms — Figure 4.

EBV Infection cycle in B cells of systemic autoimmune diseases. Author Contributions All authors contributed to the article and approved the submitted version. Conflict of Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Acknowledgments We acknowledge the contributions of all students and collaborators, who have participated in our studies on SADs.

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