CHRONIC EPSTEIN BARR VIRUS INFECTION AND CHRONIC FATIGUE SYNDROME

这个项目的目标是描述严重的慢性感染的特征。 与爱泼斯坦-巴尔病毒(EBV)的关系，并从多个方面描述 慢性疲劳综合症，早先被认为与 EB病毒感染。到目前为止，这项研究项目已经涉及到近190人 病人。包括7名被诊断为严重慢性阻塞性肺疾病的患者 EB病毒感染的临床、组织分子和病理基础 血清学特征。我们继续检查其免疫学特征。 患有严重的慢性EB病毒相关淋巴增殖和 探索治疗方法。阿昔洛韦、α和伽马干扰素已被证实 没有什么价值，但免疫抑制疗法的使用效果很好 长期的结果。 详细的免疫学、神经学、内分泌学和心理学研究 正在对选定的慢性疲劳症患者进行研究。到目前为止我们 仍然没有一致的实验室异常，允许明确的 然而，我们一直在寻求慢性疲劳综合症的诊断 神经精神病学群体异常的基础和意义， 免疫和内分泌系统。一系列关于脑垂体的研究- 肾上腺对促肾上腺皮质激素释放激素和ACTH的反应性 脊髓液中神经肽和儿茶酚水平提示一种新的 神经内分泌缺陷，可能表明中枢CRH释放不足。 由于CRH诱导中枢神经系统唤醒，这些神经内分泌发现提示了一种新的 慢性疲劳综合征患者嗜睡的机制可能是 解释过了。我们正在一系列新的研究中继续进行这些观察。 和一个新的病人队列。精氨酸-加压素输液正在进行 给予刺激和测试HPA轴。一项安慰剂对照试验 氢化可的松治疗已经开始。它应该允许我们测试 认为皮质激素缺乏会导致症状的假说。我们也 慢性疲劳综合征患者淋巴细胞表型和细胞表型的离散异常 有丝分裂原在体外对轻度免疫模式的反应 激活。幼稚(CD4xCD45RA)T细胞减少， 携带黏附标记的记忆(CD4xCD45RO)T细胞增加(LFA3， CD29等)。

The goals of this project are to characterize severe chronic infections with Epstein Barr Virus (EBV) and to characterize multiple aspects of the chronic fatigue syndrome which was, earlier, considered to be related to EBV infection. To date this research project has involved nearly 190 patients. Included are 7 patients who were diagnosed with severe chronic EBV infections on the basis of clinical, histological molecular and serologic features. We continue to examine immunologic features of patients with severe chronic EBV-associated lymphoproliferation and explore treatments. Acyclovir, alpha and gamma interferons proved of little value, but immunosuppressive therapies are being used with good long term results. Detailed immunologic, neurologic, endocrinologic and psychologic studies are being conducted on selected patients with chronic fatigue. To date we still have no consistent laboratory abnormality that permits a clear diagnosis of the chronic fatigue syndrome, however, we have been pursuing the basis and meaning of the group abnormalities in neuropsychiatric, immune and endocrine systems. A series of studies of the pituitary- adrenal responsiveness to corticotropin releasing hormone and ACTH and of neuropeptide and catechol levels in spinal fluid suggest a novel neuroendocrine defect that may indicate deficient central CRH release. Since CRH induces CNS arousal, these neuroendocrine findings suggest a new mechanism whereby the lethargy of Chronic Fatigue Syndrome patients may be explained. We are pursuing these observations in a new series of studies and a fresh patient cohort. Arginine-Vasopressin infusions are being given to stimulate and test the HPA axis. A placebo-controlled trial of hydrocortisone treatment has begun. It should permit us to test the hypothesis that corticosteroid deficit leads to symptoms. We also recognized discrete abnormalities in CFS patient lymphocyte phenotype and in vitro responsiveness to mitogens in patterns suggesting mild immune activation. There is a reduction in naive (CD4xCD45RA) T cells and an increase in memory (CD4xCD45RO) T cells bearing adhesion markers (LFA3, CD29, etc.).