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。 伴随着EB病毒(EBV)和其他淋巴增生性疾病， 并阐明慢性疲劳综合征的多个方面 早些时候被认为与EBV感染有关。到目前为止 这项研究项目涉及300多名患者。包括9名患者 谁被诊断出患有严重的慢性EBV感染 临床、组织学、分子和血清学特征。我们继续 检测重度慢性EBV患者的免疫学特征 相关淋巴增殖并探索治疗方法。阿昔洛韦，阿尔法 而伽马干扰素被证明价值不大，但具有免疫抑制作用 正在使用的治疗方法取得了良好的长期效果。 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， 我们仍然没有发现一致的实验室异常情况 慢性疲劳综合征的诊断。一系列早期研究 提示中枢CRH释放不足。自.以来 CRH诱导中枢神经系统兴奋，这些神经内分泌发现提示一种新的 慢性疲劳综合征患者嗜睡的机制可能 被解释清楚。我们正在进行一系列新的观察 研究和新的病人队列。精氨酸-血管加压素输注 给予CFS患者和对照组刺激和测试HPA轴和 数据正在分析中，70人中有62人参加了安慰剂试验- 氢化可的松治疗的对照试验。它应该允许我们 测试皮质类固醇缺乏会导致症状的假设。我们 完成了一项研究，表明CFS症状没有季节性， 进一步将其与季节性情感障碍区分开来。我们 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。我们注意到幼稚T细胞的减少和 带有黏附标记的记忆T细胞。我们已经开始追求这些 一种新的CFS类型人群的发现和相关免疫研究 在队列和急性流感患者中。一个充满活力的， 对该综合征的多学科研究仍在继续。

The goals of this project are to characterize severe chronic infections with Epstein Barr Virus (EBV) and other lymphoproliferative disorders, and to elucidate multiple aspects of the chronic fatigue syndrome which was, earlier, considered to be related to EBV infection. To date this research project has involved over 300 patients. Included are 9 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. A series of earlier studies of the pituitary-adrenal suggested 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-Vasopression infusions were given to CFS patients and controls to stimulate and test the HPA axis and the data are under analysis, 62 of 70 desired were enrolled in a placebo- controlled trial of hydrocortisone treatment. It should permit us to test the hypothesis that corticosteroid deficit leads to symptoms. We completed a study showing the absence of seasonality in CFS symptoms, further distinguishing the it from Seasonal Affective Disorder. We recognized discrete abnormalities in CFS patient lymphocyte phenotype and in vitro responsiveness to mitogens in patterns suggesting mild immune activation. We noted a reduction in naive T Cells and an increase in memory T cell bearing adhesion markers. We have begun to pursue these findings and related immune studies in populations a new CFS patint cohort and in patients with acute influenza. A vigorous, multidisciplinary approach to the syndrome continues.