Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions

被引：87

作者：

Klimas N.G. ^{[1
]}

Koneru A.O. ^{[1
]}

机构：

[1] University of Miami Miller School of Medicine, VA Medical Center, 200 BMRC, Miami, FL 33125

来源：

Current Rheumatology Reports | 2007年 / 9卷 / 6期

关键词：

Chronic Fatigue Syndrome; Serum Zinc; Infectious Mononucleosis; Valganciclovir; Chronic Fatigue Syndrome Patient;

D O I：

10.1007/s11926-007-0078-y

中图分类号：

学科分类号：

摘要：

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. Copyright © 2007 by Current Medicine Group LLC.

引用

页码：482 / 487

页数：5

共 29 条

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