Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome.
Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome.
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DOI：
10.3389/fimmu.2021.656797
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发表时间：
2021
影响因子：
7.3
通讯作者：
Zabaleta A
中科院分区：
文献类型：
--
作者：
Ruiz-Pablos M;Paiva B;Montero-Mateo R;Garcia N;Zabaleta A
肌痛性脑脊髓炎或慢性疲劳综合征（ME/CFS）影响大约1%的普通人群。它是一种慢性、致残、多系统疾病，目前尚无有效的治疗方法。这可能与人们对其起源的了解有限有关。本文就ME/CFS的发病机制进行综述，并对eb病毒（EBV）感染的免疫病理机制进行综述。鉴于EBV相关自身免疫性疾病和癌症在EBV潜伏期细胞的T细胞监测差、外周血中EBV感染细胞扩增和EBV抗体增加等方面的相似之处，我们假设EBV潜伏期细胞逃避免疫监测可能产生共同的病因。尽管尚无定论，但对ME/CFS患者的多项研究表明，细胞免疫改变和Th2反应增强可能是由于逃避某些病原体（如EBV）的机制造成的，EBV已被确定为ME/CFS患者亚群的危险因素。也就是说，具有潜伏性的细胞可能会逃避具有ME/CFS遗传易感性的个体的免疫系统，因此，CD4 T细胞对有丝分裂原和其他特定抗原的免疫力可能较差，正如在某些个体中所描述的那样。最终，我们假设在ME/CFS中存在一个具有DRB1和DQB1等位基因的亚组患者可能对EBV具有更大的易感性，其中具有潜伏期的细胞产生的免疫逃避机制诱导免疫缺陷。因此，我们提出新的努力，以研究抗ebv治疗是否可以有效地选择ME/CFS患者。
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.
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DOI：
10.1093/rheumatology/keq159
发表时间：
2010-10
期刊：
Rheumatology (Oxford, England)
影响因子：
--
作者：
Magnusson M;Brisslert M;Zendjanchi K;Lindh M;Bokarewa MI
通讯作者：
Bokarewa MI
DOI：
10.1016/j.bbi.2010.04.012
发表时间：
2010-10
期刊：
Brain, behavior, and immunity
影响因子：
--
作者：
Broderick G;Fuite J;Kreitz A;Vernon SD;Klimas N;Fletcher MA
通讯作者：
Fletcher MA
影响因子：
17.3
作者：
Collin, Simon M.;Bakken, Inger J.;White, Peter D.
通讯作者：
White, Peter D.
影响因子：
2.6
作者：
Chu, Lily;Valencia, Ian J.;Montoya, Jose G.
通讯作者：
Montoya, Jose G.
影响因子：
3.7
作者：
Bonvicini F;Manaresi E;Di Furio F;De Falco L;Gallinella G
通讯作者：
Gallinella G