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Epstein-Barr virus
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==In human disease== Epstein-Barr virus has been associated with a wide number of immune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[systemic lupus erythematosus]],<ref name="Lossius2012">{{Cite journal | title = Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation | date = December 2012| url = https://www.mdpi.com/1999-4915/4/12/3701|journal=Viruses|volume=4|issue=12 | pages = 3701–3730 | last = Lossius | first = Andreas | author-link = | last2 = Johansen | first2 = Jorunn N. | authorlink2 = | last3 = Torkildsen | first3 = Øivind | authorlink3 = | last4 = Vartdal | first4 = Frode | authorlink4 = | last5 = Holmøy | first5 = Trygve | authorlink5 = |language=en|doi=10.3390/v4123701|pmc=PMC3528287|pmid=|issn=1999-4915|via=|quote=}}</ref> c[[Chronic fatigue syndrome|hronic fatigue syndrome]], and [[myasthenia gravis]]. EBV was recently discovered to turn on "risk genes" for autoimmune disease in the cells it infects. [[Epstein-Barr virus nuclear antigen 2|EBNA2]], a protein produced by EBV-infected cells, and its related transcription factors activate half the human genes known to be associated with the risk for lupus as well as genes associated with several other autoimmune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[inflammatory bowel disease]], [[Diabetes#Types|type 1 diabetes]], [[juvenile idiopathic arthritis]] and [[celiac disease]]. EBV activation can thus increase the risk of developing these diseases.<ref name="Harley2018" /><ref name="NIHNews2018" /> ===Chronic fatigue syndrome=== A prospective study of 250 primary care patients revealed a higher prevalence of [[chronic fatigue syndrome]] after infectious [[mononucleosis]] (glandular fever) when compared to an ordinary upper respiratory tract infection.<ref name="White1998">{{Cite journal | last = White | first = P.D. | last2 = Thomas | first2 = J.M. | last3 = Amess | first3 = J. | last4 = Crawford | first4 =D.H. | last5 = Grover | first5 = S.A. | last6 = Kangro | first6 = H.O. | last7 = Clare | first7 = A.W. | date = Dec 1998 | title = Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever |url =https://www.ncbi.nlm.nih.gov/pubmed/9926075|journal=The British Journal of Psychiatry: The Journal of Mental Science|volume=173 | pages = 475–481|issn=0007-1250|pmid=9926075|issue=|doi=|pmc=|quote= | author-link = Peter White|via=}}</ref> Anti-early antigen titers to EBV were elevated in CFS patients and associated with worse symptoms.<ref name="Schmaling1996">{{Cite journal | last = Schmaling | first = K.B. | last2 = Jones | first2 = J.F. | date = Jan 1996 | title = MMPI profiles of patients with chronic fatigue syndrome | url =https://www.ncbi.nlm.nih.gov/pubmed/8730646|journal=Journal of Psychosomatic Research|volume=40|issue=1 | pages = 67–74|issn=0022-3999|pmid=8730646}}</ref> A 2006 Australian prospective study found that 12% of subjects infected by EBV met the criteria for [[chronic fatigue syndrome]] six months after their infection, and 9% still had CFS 12 months after infection.<ref name="Hickie2006">{{Cite journal | last = Hickie | first = Ian | author-link = Ian Hickie | last2 = Davenport | first2 = Tracey | authorlink2 = Tracey Davenport | last3 = Wakefield | first3 = Denis | authorlink3 = Denis Wakefield | last4 = Vollmer-Conna | first4 = Ute | authorlink4 = Uté Vollmer-Conna | last5 = Cameron | first5 = Barbara | authorlink5 = | last6 = Vernon | first6 = Suzanne D | authorlink6 = Suzanne Vernon | last7 = Reeves | first7 = William C | author-link8 = William Reeves | last8 = Lloyd | first8 = Andrew | author-link8 = Andrew Lloyd | date = 2006-09-16 | title = Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study| url = https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569956/|journal=BMJ : British Medical Journal|volume=333|issue=7568 | pages = 575|doi=10.1136/bmj.38933.585764.AE|issn=0959-8138|pmc=1569956|pmid=16950834|access-date=|quote=|via=}}</ref> (The same rate held true for [[Ross River virus]] and [[Q fever]].) In another study sample, 110 of 178 patients with increased antibodies against EBV had a diagnosis of CFS.<ref name="Mikirova2014" /> === Long COVID === Long COVID may be associated [[herpesvirus]] reactivation such as EBV.<ref>{{Cite journal | last = Proal | first = Amy D. | authorlink = Amy Proal | last2 = VanElzakker | first2 = Michael B. | authorlink2 = Michael VanElzakker | date = 2021 | title=Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms |url =https://www.frontiersin.org/articles/10.3389/fmicb.2021.698169/full|journal=Frontiers in Microbiology|language=English|volume=12|issue= | pages = 698169|doi=10.3389/fmicb.2021.698169|issn=1664-302X}}</ref><ref name=":0">{{Cite journal | title = Investigation of Long COVID Prevalence and Its Relationship to Epstein-Barr Virus Reactivation | date = June 2021| url = https://www.mdpi.com/2076-0817/10/6/763/htm|journal=Pathogens|volume=10|issue=6 | pages = 763 | last = Gold | first = Jeffrey E. | authorlink = | last2 = Okyay | first2 = Ramazan A. | authorlink2 = | last3 = Licht | first3 = Warren E. | author-link3 = | last4 = Hurley | first4 = David J. | author-link4 = | last5 = | first5 = | authorlink5 = | last8 = | first8 = |language=en|doi=10.3390/pathogens10060763|pmc=|pmid=|access-date=|issn=2076-0817|quote=|via=}}</ref> ===Multiple sclerosis=== Infection later in life, high serum titers against EBV, and [[mononucleosis]] have all been associated with an increased risk of multiple sclerosis. MS relapses are correlated with EBV reactivation.<ref name="Holmoy2008">{{Cite journal | title = Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis | date = 2008-01-01| url = https://www.sciencedirect.com/science/article/pii/S0306987707003167|journal=Medical Hypotheses|volume=70|issue=1 | pages = 66–69 | last = Holmøy | first = Trygve|language=en|doi=10.1016/j.mehy.2007.04.030|issn=0306-9877}}</ref> Several studies by Alberto Ascherio, MD, DrPH, and his team at the Harvard School of Public Health have suggested that EBV is involved in [[multiple sclerosis]], specifically in people with a certain immune-related gene and high levels of antibodies to EBV in their blood.<ref>{{Cite web | url=https://www.nationalmssociety.org/What-is-MS/What-Causes-MS/Viruses | title = Viruses | last = | first = | date = |website=National Multiple Sclerosis Society|archive-url=|archive-date=|url-status=|access-date=2018-11-14}}</ref> === Systemic lupus erythematosus === In a study of young patients with lupus, 99% had EBV as compared to 70% of healthy controls.<ref name="James1997">{{Cite journal | title = An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus. | date = 1997-12-15| url = https://www.jci.org/articles/view/119856|journal=The Journal of Clinical Investigation|volume=100|issue=12 | pages = 3019–3026 | last = James | first = J.A. | last2 = Kaufman | first2 = K.M. | last3 = Farris | first3 = A.D. | last4 = Taylor-Albert | first4 = E. | last5 = Lehman | first5 = T.J. | last6 = Harley | first6 = J.B.|language=en|doi=10.1172/JCI119856|pmid=9399948|issn=0021-9738}}</ref> Another study found that patients with systemic lupus erythematosus had a roughly 40-fold increase in EBV viral loads compared with controls, likely stemming from altered [[t cell]] responses against EBV.<ref>{{Cite journal | title = Defective Control of Latent Epstein-Barr Virus Infection in Systemic Lupus Erythematosus | date = 2004-01-15| url = https://www.jimmunol.org/content/172/2/1287|journal=The Journal of Immunology|volume=172|issue=2 | pages = 1287–1294 | last = Kang | first = Insoo | last2 = Quan | first2 = Timothy | last3 = Nolasco | first3 = Helena | last4 = Park | first4 = Sung-Hwan | last5 = Hong | first5 = Myung Sun | last6 = Crouch | first6 = Jill | last7 = Pamer | first7 = Eric G. | last8 = Howe | first8 = John Greg | last9 = Craft | first9 = Joe|language=en|doi=10.4049/jimmunol.172.2.1287|pmid=14707107|issn=0022-1767}}</ref> ===Myasthenia gravis=== [[Myasthenia gravis]] is an [[autoimmune disease]] which has been associated with a large number of different viruses, particularly EBV, [[Human papillomavirus|HPV]], and [[Poliovirus|polioviruses]]. In several studies EBV infection of the thymus has been found in myasthenia gravis patients, but not all studies have found this.<ref name=":1">{{Cite journal | title = A Systematic Review of the Potential Implication of Infectious Agents in Myasthenia Gravis | date = 2021 | url=https://www.frontiersin.org/article/10.3389/fneur.2021.618021|journal=Frontiers in Neurology|volume=12 | last = Leopardi | first = Victoria | last2 = Chang | first2 = Yu-Mei | last3 = Pham | first3 = Andrew | last4 = Luo | first4 = Jie | last5 = Garden | first5 = Oliver A.|doi=10.3389/fneur.2021.618021/full|issn=1664-2295}}</ref> [[B cell|B cells]] from [[myasthenia gravis]] patients stimulated ''in vitro'' by Epstein-Barr virus produced [[acetylcholine]] autoantibodies.<ref>{{Cite journal | last = Brenner | first = T. | last2 = Timore | first2 = Y. | last3 = Wirguin | first3 = I. | last4 = Abramsky | first4 = O. | last5 = Steinitz | first5 = M. | date = Oct 1989 | title = In vitro synthesis of antibodies to acetylcholine receptor by Epstein-Barr virus-stimulated B-lymphocytes derived from patients with myasthenia gravis |url =https://www.ncbi.nlm.nih.gov/pubmed/2553772|journal=Journal of Neuroimmunology|volume=24|issue=3 | pages = 217–222|issn=0165-5728|pmid=2553772}}</ref> While EBV infection of the [[thymus]] has been posited as a causative agent for the production of [[acetylcholine]] receptor autoantibodies in [[myasthenia gravis]].<ref>{{Cite journal | last = Kaminski | first = Henry J | last2 = Minarovits | first2 = Janos | title = Epstein-barr virus: Trigger for autoimmunity?| url = http://www.academia.edu/20258853/Epstein-barr_virus_Trigger_for_autoimmunity/|journal=Annals of Neurology|language=en|issn=0364-5134 | date = 2010 | volume=67|issue=6 | pages = 697-698| doi = | pmc = | pmid = | quote = |access-date=|via=}}</ref>, there is only limited evidence supporting EBV or other viruses as a cause of myasthenia gravis.<ref name=":1" /> === Gastrointestinal disease === One study of EBV in patients with [[gastritis]], [[Crohn's disease]], and [[ulcerative colitis]] and normal controls found essentially undetectable levels of EBV in normal gastric mucosa. However, EBV was detected in 46% of gastritis lesions, 44% of normal colonic mucosa, 55% of Crohn’s disease, and 64% of ulcerative colitis samples.<ref>{{Cite journal | title = Epstein-Barr Virus Infection Is Common in Inflamed Gastrointestinal Mucosa | date = 2012-07-01| url = https://doi.org/10.1007/s10620-012-2116-5|journal=Digestive Diseases and Sciences|volume=57|issue=7 | pages = 1887–1898 | last = Ryan | first = Julie L. | last2 = Shen | first2 = You-Jun | last3 = Morgan | first3 = Douglas R. | last4 = Thorne | first4 = Leigh B. | last5 = Kenney | first5 = Shannon C. | last6 = Dominguez | first6 = Ricardo L. | last7 = Gulley | first7 = Margaret L.|language=en|doi=10.1007/s10620-012-2116-5|pmc=PMC3535492|pmid=22410851|issn=1573-2568}}</ref> ===Lyme disease=== Several herpesviruses including Epstein-Barr virus may cause false positives on [[Lyme disease]] tests.<ref name="Goossens1999">{{Cite journal | last1 = Goossens | first1 = HA | last2 = Nohlmans | first2 = MK | last3 = van den Bogaard | first3 = AE | title = Epstein-Barr virus and cytomegalovirus infections cause false-positive results in IgM two-test protocol for early Lyme borreliosis| journal = Infection | date = May-Jun 1999 | volume = 27 | issue = 3| pages =231| doi = 10.1007/BF02561539 | pmid = 10378140| url = https://www.ncbi.nlm.nih.gov/pubmed/10378140}}</ref> ===XMEN disease=== A 2014 study found chronic Epstein-Barr infection was linked to a magnesium transporter [[magnesium transporter 1|MAGT]] mutation.<ref name="MAGT1">{{Cite web | url=https://www.ncbi.nlm.nih.gov/gene/84061 | title = MAGT1 magnesium transporter 1 [Homo sapiens (human)] | last = | first = | authorlink = | date = | website = NCBI|archive-url=|archive-date=|url-status=|access-date=2022-05-21}}</ref> Dysfunction in this transporter also resulted in decreased NK cell function, and neoplasia (sometimes-cancerous growths).<ref name="X-men_disease_1">{{Cite journal | last1 = Li | first1 = F.-Y. | author-link1 = | last2 = Chaigne-Delalande | first2 = B | authorlink2 = | last3 = Su | first3 = H | last4 = Matthews | first4 = H | last5 = Lenardo |first5 = M.J. | authorlink3 = | title = XMEN disease: a new primary immunodeficiency affecting Mg2+ regulation of immunity against Epstein-Barr virus. | journal =Blood| date = 2014| doi = 10.1182/blood-2013-11-538686| url = https://ashpublications.org/blood/article/123/14/2148/32463/XMEN-disease-a-new-primary-immunodeficiency|volume=123|issue=14 | pages = 2148–2152|pmc=|pmid=|quote=|via=}}</ref> This disorder, termed "XMEN" (for X-linked, EBV, and neoplasia) was identified as a recessive, X-linked disorder that would therefore be many times more common in men. Since chronic EBV infection has been associated with chronic fatigue syndrome, this error in [[magnesium]] transport may be worth considering in male patients, especially with slow onset and history of childhood infection.<ref name="X-men_disease_1" /><ref name="X-men_disease_2">{{Cite journal | title = X-linked immunodeficiency with magnesium defect, Epstein–Barr virus infection, and neoplasia disease: a combined immune deficiency with magnesium defect | date = Dec 2014| url = https://journals.lww.com/co-pediatrics/Abstract/2014/12000/X_linked_immunodeficiency_with_magnesium_defect,.16.aspx|journal=Current Opinion in Pediatrics|volume=26|issue=6 | pages = 713–719 | last = Ravell | first = Juan | author-link = | last2 = Chaigne-Delalande | first2 = Benjamin | authorlink2 = | last3 = Lenardo | first3 = Michael | authorlink3 = |language=en-US|doi=10.1097/MOP.0000000000000156|pmc=PMC4306042|pmid=25313976|access-date=|issn=1040-8703|quote=|via=}}</ref> However, in this disorder, EBV would be seen as an indicator of the illness rather than the cause.
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