Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome

Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) affects approximately 1% of the general population. It is a chronic, disabling, multi-system disease for which there is no effective treatment. This is probably related to the limited knowledge about its origin. Here, we summarized the c...

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Autores principales: Manuel Ruiz-Pablos, Bruno Paiva, Rosario Montero-Mateo, Nicolas Garcia, Aintzane Zabaleta
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Publicado: Frontiers Media S.A. 2021
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spelling oai:doaj.org-article:40b36b3f5a574fb7adff4134fe44b6a42021-11-15T06:50:34ZEpstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome1664-322410.3389/fimmu.2021.656797https://doaj.org/article/40b36b3f5a574fb7adff4134fe44b6a42021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.656797/fullhttps://doaj.org/toc/1664-3224Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) affects approximately 1% of the general population. It is a chronic, disabling, multi-system disease for which there is no effective treatment. This is probably related to the limited knowledge about its origin. Here, we summarized the current knowledge about the pathogenesis of ME/CFS and revisit the immunopathobiology of Epstein-Barr virus (EBV) infection. Given the similarities between EBV-associated autoimmune diseases and cancer in terms of poor T cell surveillance of cells with EBV latency, expanded EBV-infected cells in peripheral blood and increased antibodies against EBV, we hypothesize that there could be a common etiology generated by cells with EBV latency that escape immune surveillance. Albeit inconclusive, multiple studies in patients with ME/CFS have suggested an altered cellular immunity and augmented Th2 response that could result from mechanisms of evasion to some pathogens such as EBV, which has been identified as a risk factor in a subset of ME/CFS patients. Namely, cells with latency may evade the immune system in individuals with genetic predisposition to develop ME/CFS and in consequence, there could be poor CD4 T cell immunity to mitogens and other specific antigens, as it has been described in some individuals. Ultimately, we hypothesize that within ME/CFS there is a subgroup of patients with DRB1 and DQB1 alleles that could confer greater susceptibility to EBV, where immune evasion mechanisms generated by cells with latency induce immunodeficiency. Accordingly, we propose new endeavors to investigate if anti-EBV therapies could be effective in selected ME/CFS patients.Manuel Ruiz-PablosBruno PaivaRosario Montero-MateoNicolas GarciaAintzane ZabaletaFrontiers Media S.A.articlechronic fatigue syndromemyalgic encephalomyelitisEBV EBNA-1HLA-II allelescancerCD4+ CTLImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic chronic fatigue syndrome
myalgic encephalomyelitis
EBV EBNA-1
HLA-II alleles
cancer
CD4+ CTL
Immunologic diseases. Allergy
RC581-607
spellingShingle chronic fatigue syndrome
myalgic encephalomyelitis
EBV EBNA-1
HLA-II alleles
cancer
CD4+ CTL
Immunologic diseases. Allergy
RC581-607
Manuel Ruiz-Pablos
Bruno Paiva
Rosario Montero-Mateo
Nicolas Garcia
Aintzane Zabaleta
Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
description Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) affects approximately 1% of the general population. It is a chronic, disabling, multi-system disease for which there is no effective treatment. This is probably related to the limited knowledge about its origin. Here, we summarized the current knowledge about the pathogenesis of ME/CFS and revisit the immunopathobiology of Epstein-Barr virus (EBV) infection. Given the similarities between EBV-associated autoimmune diseases and cancer in terms of poor T cell surveillance of cells with EBV latency, expanded EBV-infected cells in peripheral blood and increased antibodies against EBV, we hypothesize that there could be a common etiology generated by cells with EBV latency that escape immune surveillance. Albeit inconclusive, multiple studies in patients with ME/CFS have suggested an altered cellular immunity and augmented Th2 response that could result from mechanisms of evasion to some pathogens such as EBV, which has been identified as a risk factor in a subset of ME/CFS patients. Namely, cells with latency may evade the immune system in individuals with genetic predisposition to develop ME/CFS and in consequence, there could be poor CD4 T cell immunity to mitogens and other specific antigens, as it has been described in some individuals. Ultimately, we hypothesize that within ME/CFS there is a subgroup of patients with DRB1 and DQB1 alleles that could confer greater susceptibility to EBV, where immune evasion mechanisms generated by cells with latency induce immunodeficiency. Accordingly, we propose new endeavors to investigate if anti-EBV therapies could be effective in selected ME/CFS patients.
format article
author Manuel Ruiz-Pablos
Bruno Paiva
Rosario Montero-Mateo
Nicolas Garcia
Aintzane Zabaleta
author_facet Manuel Ruiz-Pablos
Bruno Paiva
Rosario Montero-Mateo
Nicolas Garcia
Aintzane Zabaleta
author_sort Manuel Ruiz-Pablos
title Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
title_short Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
title_full Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
title_fullStr Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
title_full_unstemmed Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
title_sort epstein-barr virus and the origin of myalgic encephalomyelitis or chronic fatigue syndrome
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/40b36b3f5a574fb7adff4134fe44b6a4
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AT brunopaiva epsteinbarrvirusandtheoriginofmyalgicencephalomyelitisorchronicfatiguesyndrome
AT rosariomonteromateo epsteinbarrvirusandtheoriginofmyalgicencephalomyelitisorchronicfatiguesyndrome
AT nicolasgarcia epsteinbarrvirusandtheoriginofmyalgicencephalomyelitisorchronicfatiguesyndrome
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