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by L.D. Devanur and J.R. Kerr
December 13, 2006
Journal: Journal of Clinical Virology. 2006 Nov; 37(3):139-50. [E-publication 2006 Sep 15.]
Authors and affiliation: Devanur LD, Kerr JR. Chronic Fatigue Syndrome (CFS) Group, Department of Cellular & Molecular Medicine, St. George's University of London, London, UK. [E-mail: jkerr@sgul.ac.uk ]
PMID: 16978917
Chronic Fatigue Syndrome (CFS) is thought to have a worldwide prevalence of 0.4 percent to 1.0 percent, with approximately 240,000 patients in the UK.
Diagnosis is based on clinical criteria and critically depends on exclusion of other physical and psychiatric diseases.
Studies of pathogenesis have revealed immune system abnormalities and chronic immune activation, dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, brain abnormalities, evidence of emotional stress (comprising host aspects) and evidence of exogenous insults, for example, various microbial infections (Epstein-Barr virus, enteroviruses, parvovirus B19, Coxiella burnetii and Chlamydia pneumoniae), vaccinations, and exposure to organophosphate chemicals and other toxins (comprising environmental aspects).
Emotional stress appears to be very important as it reduces the ability of the immune system to clear infections, it's presence has been shown to determine whether or not an individual develops symptoms upon virus infection, and it leads to activation of the HPA axis.
But, emotional stress is distinct from depression, the presence of which precludes a diagnosis of CFS. There is no specific treatment for CFS other than the much underutilized approach of specific treatment of virus infections.
Current priorities are to understand the molecular pathogenesis of disease in terms of human and virus gene expression, to develop a diagnostic test based on protein biomarkers, and to develop specific curative treatments.
Keywords: Chronic fatigue syndrome; Virus; Infection; Diagnosis; Pathogenesis;
Gene expression
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