Faculty Articles
Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions
Publication Title
Current Rheumatology Reports
ISSN
1523-3774
Publication Date
12-1-2007
Abstract
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.
Volume
9
Issue
6
First Page
482
Last Page
487
Disciplines
Medical Specialties | Medicine and Health Sciences | Osteopathic Medicine and Osteopathy
NSUWorks Citation
Klimas, Nancy G. and Koneru, A. O., "Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions" (2007). Faculty Articles. 448.
https://nsuworks.nova.edu/hpd_com_faculty_articles/448