Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome
| Autor: | Bruno Paiva, Rosario Montero-Mateo, Manuel Ruiz-Pablos, Nicolás García, Aintzane Zabaleta |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
musculoskeletal diseases
CD4-Positive T-Lymphocytes Cellular immunity Epstein-Barr Virus Infections Herpesvirus 4 Human T cell Mini Review Population Immunology Human leukocyte antigen medicine.disease_cause Lymphocyte Activation chronic fatigue syndrome CD4+ CTL Immune system Chronic fatigue syndrome Immunology and Allergy Medicine Humans cancer Genetic Predisposition to Disease education Antigens Viral Immunodeficiency education.field_of_study B-Lymphocytes HLA-D Antigens Immunity Cellular Fatigue Syndrome Chronic Infecciones por virus de Epstein-Barr business.industry HLA-II alleles autoimmunity Models Immunological Cáncer RC581-607 medicine.disease Epstein–Barr virus Virus myalgic encephalomyelitis medicine.anatomical_structure EBV EBNA-1 immunotherapy Immunologic diseases. Allergy business Enfermedad |
| Zdroj: | Frontiers in Immunology Frontiers in Immunology, Vol 12 (2021) ABACUS. Repositorio de Producción Científica Universidad Europea (UEM) |
| ISSN: | 1664-3224 |
| Popis: | 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. Ramsay Award Program 2019 Cycle from the Solve ME/ CFS Initiative 7.561 JCR (2020) Q1, 24/162 Immunology 2.646 SJR (2020) Q1, 27/213 Immunology No data IDR 2020 UEM |
| Databáze: | OpenAIRE |
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