Chronic fatigue syndrome: inflammation, immune function, and
neuroendocrine interactions.
Journal: Curr Rheumatol Rep. 2007 Dec;9(6):482-7.
Authors: Klimas NG, Koneru AO.
Affiliation: University of Miami Miller School of Medicine, 1201 NW
16th Street, VA Medical Center, 200 BMRC, 6th Floor, Miami, FL 33125,
USA. nancy.klimas@va.gov
NLM Citation: PMID: 18177602
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.
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