Chronic Fatigue Syndrome: Inflammation, immune function, and neuroendocrine interactions – Source: Current Rheumatology Reports, Dec 2007

Investigations into the underlying cause of Chronic Fatigue Syndrome have advanced the field considerably in the past year.

n Gene microarray data have led to a better understanding of pathogenesis.

n Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments.

n Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue.

n Genomic studies showed that persistent cases express Epstein Barr virus-specific genes and demonstrate abnormalities of mitochondrial function.

n 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.

n 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.

Source: Current Rheumatology Reports. 2007 Dec;9(6):482-7. PMID: 18177602, by Nancy G. Klimas, MD and AO Koneru, MD. University of Miami Miller School of Medicine, VA Medical Center, Miami, Florida, USA. [E-mail:]

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