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We have previously reported genomic subtypes of CFS/ME based on expression of 88 human genes. In this study we attempted to:
• Reproduce these findings,
• Determine specificity of this signature to CFS/ME,
• And test for associations between CFS/ME subtype and infection.
We determined expression levels of 88 human genes in blood of:
• 61 new patients with idiopathic [cause undefined] CFS/ME (according to Fukuda criteria),
• 6 patients with Q-fever associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria),
• 14 patients with endogenous [likely genetic] depression (according to DSM-IV criteria), and
• 18 normal blood donors.
In patients with CFS/ME, differential expression was confirmed for all 88 genes.
• Q-CFS/ME patients had similar patterns of gene expression to idiopathic CFS/ME.
• Gene expression in endogenous depression patients was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2, PDCD6).
Clustering of combined gene data in CFS/ME patients for this and our previous study (n=117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF-36 scores, clinical phenotypes [observable traits], severity and geographical distribution.
Antibody testing for Epstein-Barr virus (EBV), enterovirus, Coxiella burnetii and parvovirus B19 revealed subtype-specific relationships for EBV and enterovirus, the two most common infectious triggers of CFS/ME.
Source: Journal of Clinical Pathology, Dec 2, 2009. PMID: 19955554, by Zhang L, Goudh J, Christmas D, Mattey D, Richards S, Main J, Enlander D, Honeybourne D, Ayres J, Nutt DJ, Kerr J. St George’s University of London; University of Bristol, Staffordshire Rheumatology Centre; Poole Hospital NHS Trust; Imperial College London; New York ME/CFS Service (UK); University of Birmingham, UK. [E-mail: firstname.lastname@example.org]