Epstein–Barr virus–associated lymphoproliferative diseases

Epstein–Barr virus–associated lymphoproliferative diseases
Other namesEBV-associated lymphoproliferative diseases
Electron micrograph of two Epstein–Barr virions (viral particles) showing round capsids loosely surrounded by the membrane envelope
SpecialtyHematology, oncology, infectious disease, virology
CausesEpstein–Barr virus

Epstein–Barr virus–associated lymphoproliferative diseases (also abbreviated EBV-associated lymphoproliferative diseases or EBV+ LPD) are a group of disorders in which one or more types of lymphoid cells (a type of white blood cell), i.e. B cells, T cells, NK cells, and histiocytic-dendritic cells, are infected with the Epstein–Barr virus (EBV). This causes the infected cells to divide excessively, and is associated with the development of various non-cancerous, pre-cancerous, and cancerous lymphoproliferative disorders (LPDs). These LPDs include the well-known disorder occurring during the initial infection with the EBV, infectious mononucleosis, and the large number of subsequent disorders that may occur thereafter. The virus is usually involved in the development and/or progression of these LPDs although in some cases it may be an "innocent" bystander, i.e. present in, but not contributing to, the disease.[1]

EBV-associated LPDs are a subcategory of EBV-associated diseases. Non-LPD that have significant percentages of cases associated with EBV infection (see Epstein–Barr virus infection) include the immune disorders of multiple sclerosis[2] and systemic lupus erythematosus;[3] malignancies such as stomach cancers,[4] soft tissue sarcomas, leiomyosarcoma, and undifferentiated nasopharyngeal cancer;[5] the childhood disorders of Alice in Wonderland syndrome;[6] and acute cerebellar ataxia.[7]

About 50% of all five-year-old children and 90% of adults have evidence of previous infection with EBV.[8] During the initial infection, the virus may cause infectious mononucleosis, only minor non-specific symptoms, or no symptoms. Regardless of this, the virus enters a latency phase in its host and the infected individual becomes a lifetime asymptomatic carrier of EBV. Weeks, months, years, or decades thereafter, a small percentage of these carriers, particularly those with an immunodeficiency, develop an EBV+ LPD. Worldwide, EBV infection is associated with 1%[9] to 1.5%[10] of all cancers.[1] The vast majority of these EBV-associated cancers are LPD. The non-malignant, premalignant, and malignant forms of EBV+ LPD have a huge impact on world health.[1]

The classification and nomenclature of the LPD reported here follow the revisions made by the World Health Organization in 2016. This classification divides EBV+ LPD into five categories: EBV-associated reactive lymphoid proliferations, EBV-associated B cell lymphoproliferative disorders, EBV-associated NK/T cell lymphoproliferative disorders, EBV-associated immunodeficiency-related lymphoproliferative disorders, and EBV-associated histiocytic-dendritic disorders.[11]

  1. ^ a b c Rezk SA, Zhao X, Weiss LM (June 2018). "Epstein–Barr virus–associated lymphoid proliferations, a 2018 update". Human Pathology. 79: 18–41. doi:10.1016/j.humpath.2018.05.020. PMID 29885408. S2CID 47010934.
  2. ^ Bjornevik K, Cortese M, Healy BC, Kuhle J, Mina MJ, Leng Y, Elledge SJ, Niebuhr DW, Scher AI, Munger KL, Ascherio A (January 2022). "Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis". Science. 375 (6578): 296–301. Bibcode:2022Sci...375..296B. doi:10.1126/science.abj8222. PMID 35025605. S2CID 245983763.
  3. ^ Ascherio A, Munger KL (2015). "EBV and Autoimmunity". Epstein Barr Virus Volume 1. Current Topics in Microbiology and Immunology. Vol. 390. pp. 365–85. doi:10.1007/978-3-319-22822-8_15. ISBN 978-3-319-22821-1. PMID 26424654.
  4. ^ Naseem M, Barzi A, Brezden-Masley C, Puccini A, Berger MD, Tokunaga R, Battaglin F, Soni S, McSkane M, Zhang W, Lenz HJ (May 2018). "Outlooks on Epstein–Barr virus associated gastric cancer". Cancer Treatment Reviews. 66: 15–22. doi:10.1016/j.ctrv.2018.03.006. PMC 5964025. PMID 29631196.
  5. ^ Weiss RA (October 2016). "Tumour-inducing viruses". British Journal of Hospital Medicine. 77 (10): 565–568. doi:10.12968/hmed.2016.77.10.565. PMID 27723397.
  6. ^ Mastria G, Mancini V, Viganò A, Di Piero V (2016). "Alice in Wonderland Syndrome: A Clinical and Pathophysiological Review". BioMed Research International. 2016: 8243145. doi:10.1155/2016/8243145. PMC 5223006. PMID 28116304.
  7. ^ Nussinovitch M, Prais D, Volovitz B, Shapiro R, Amir J (September 2003). "Post-infectious acute cerebellar ataxia in children". Clinical Pediatrics. 42 (7): 581–4. doi:10.1177/000992280304200702. PMID 14552515. S2CID 22942874.
  8. ^ "About 90% of adults have antibodies that show that they have a current or past EBV infection". National Center for Infectious Diseases. US CDC. 28 September 2020. Archived from the original on 2016-08-08.
  9. ^ Houldcroft CJ, Kellam P (March 2015). "Host genetics of Epstein–Barr virus infection, latency and disease". Reviews in Medical Virology. 25 (2): 71–84. doi:10.1002/rmv.1816. PMC 4407908. PMID 25430668.
  10. ^ Farrell PJ (August 2018). "Epstein–Barr Virus and Cancer". Annual Review of Pathology. 14: 29–53. doi:10.1146/annurev-pathmechdis-012418-013023. PMID 30125149. S2CID 52051261.
  11. ^ Swerdlow SH, Campo E, Pileri SA, Harris NL, Stein H, Siebert R, Advani R, Ghielmini M, Salles GA, Zelenetz AD, Jaffe ES (May 2016). "The 2016 revision of the World Health Organization classification of lymphoid neoplasms". Blood. 127 (20): 2375–90. doi:10.1182/blood-2016-01-643569. PMC 4874220. PMID 26980727.
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