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Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease.
Adv Exp Med Biol 2011; 711:82-102AE

Abstract

Epstein-Barr virus (EBV) is ahumanherpesvirus thatpersists in the memory B-cells of the majority of the world population in a latent form. Primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis. Virus latency is associated with a wide variety of neoplasms whereof some occur in immune suppressed individuals. Virus production does not occur in strict latency. The expression of latent viral oncoproteins and nontranslated RNAs is under epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of a couple of latency promoters in tumor cells, germinal center B cells and lymphoblastoid cells (LCL, transformed by EBV in vitro). Both, latent and lytic EBV proteins elicit a strong immune response. In immune suppressed and infectious mononucleosis patients, an increased viral load can be detected in the blood. Enhanced lytic replication may result in new infection- and transformation-events and thus is a risk factor both for malignant transformation and the development of autoimmune diseases. An increased viral load or a changed presentation of a subset of lytic or latent EBV proteins that cross-react with cellular antigens may trigger pathogenic processes through molecular mimicry that result in multiple sclerosis (MS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Authors+Show Affiliations

Institute for Medical Microbiology and Hygiene of the University of Regensburg, Regensburg, Germany. hans-helmut.niller@klinik.uni-regensburg.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

21627044

Citation

Niller, Hans Helmut, et al. "Epigenetic Dysregulation of Epstein-barr Virus Latency and Development of Autoimmune Disease." Advances in Experimental Medicine and Biology, vol. 711, 2011, pp. 82-102.
Niller HH, Wolf H, Ay E, et al. Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease. Adv Exp Med Biol. 2011;711:82-102.
Niller, H. H., Wolf, H., Ay, E., & Minarovits, J. (2011). Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease. Advances in Experimental Medicine and Biology, 711, pp. 82-102.
Niller HH, et al. Epigenetic Dysregulation of Epstein-barr Virus Latency and Development of Autoimmune Disease. Adv Exp Med Biol. 2011;711:82-102. PubMed PMID: 21627044.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease. AU - Niller,Hans Helmut, AU - Wolf,Hans, AU - Ay,Eva, AU - Minarovits,Janos, PY - 2011/6/2/entrez PY - 2011/6/2/pubmed PY - 2011/6/10/medline SP - 82 EP - 102 JF - Advances in experimental medicine and biology JO - Adv. Exp. Med. Biol. VL - 711 N2 - Epstein-Barr virus (EBV) is ahumanherpesvirus thatpersists in the memory B-cells of the majority of the world population in a latent form. Primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis. Virus latency is associated with a wide variety of neoplasms whereof some occur in immune suppressed individuals. Virus production does not occur in strict latency. The expression of latent viral oncoproteins and nontranslated RNAs is under epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of a couple of latency promoters in tumor cells, germinal center B cells and lymphoblastoid cells (LCL, transformed by EBV in vitro). Both, latent and lytic EBV proteins elicit a strong immune response. In immune suppressed and infectious mononucleosis patients, an increased viral load can be detected in the blood. Enhanced lytic replication may result in new infection- and transformation-events and thus is a risk factor both for malignant transformation and the development of autoimmune diseases. An increased viral load or a changed presentation of a subset of lytic or latent EBV proteins that cross-react with cellular antigens may trigger pathogenic processes through molecular mimicry that result in multiple sclerosis (MS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SN - 0065-2598 UR - https://www.unboundmedicine.com/medline/citation/21627044/Epigenetic_dysregulation_of_epstein_barr_virus_latency_and_development_of_autoimmune_disease_ L2 - https://dx.doi.org/10.1007/978-1-4419-8216-2_7 DB - PRIME DP - Unbound Medicine ER -