Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions.
Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions.
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DOI：
10.1007/s11926-007-0078-y
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发表时间：
2007-12-01
影响因子：
5
通讯作者：
Koneru, Anne O'Brien
中科院分区：
文献类型：
--
作者：
Klimas, Nancy G;Koneru, Anne O'Brien
在过去的一年里，对慢性疲劳综合征的根本原因的调查大大推进了这一领域。基因微阵列数据使我们对发病机制有了更好的理解。最近的研究评估了遗传特征，描述了生物亚群，并提出了潜在的靶向治疗方法。急性病毒感染研究发现，初始感染严重程度是持续疲劳的唯一最佳预测因素。基因组研究表明，持续性病例表达爱泼斯坦巴尔病毒特异性基因，并显示线粒体功能异常。免疫功能障碍的研究通过细胞内穿孔素和颗粒酶的定量评价扩展了对细胞毒性T细胞的自然杀伤细胞毒性细胞功能障碍的观察。其他研究集中在一个亚组的患者重新激活病毒感染。这些进展应导致影响免疫功能，下丘脑-垂体-肾上腺轴调节和持续病毒再激活的靶向治疗。
Investigations into the underlying cause of chronic fatigue syndrome have advanced the field considerably in the past year. Gene microarray data have led to a better understanding of pathogenesis. Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments. Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue. Genomic studies showed that persistent cases express Epstein Barr virus-specific genes and demonstrate abnormalities of mitochondrial function. Studies of immune dysfunction extended observations of natural killer cytotoxic cell dysfunction of the cytotoxic T cell through quantitative evaluation of intracellular perforins and granzymes. Other research has focused on a subgroup of patients with reactivated viral infection. These advances should result in targeted therapies that impact immune function, hypothalamic-pituitary-adrenal axis regulation, and persistent viral reactivation.