19 January 2008
Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions
Current Rheumatology Reports, Vol. 9, #6, pp
482-487, December 2007
Nancy G. Klimas and Anne O’Brien Koneru
University of Miami Miller School of Medicine, 1201 NW 16th Street, VA Medical Center, 200 BMRC, 6th Floor, Miami, FL 33125, USA
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.