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Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis.

Zhang L, Gough J, Christmas D, Mattey DL, Richards SC, Main J, Enlander D, Honeybourne D, Ayres JG, Nutt DJ, Kerr JR - J. Clin. Pathol. (2009)

Bottom Line: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.In patients with CFS/ME, differential expression was confirmed for all 88 genes.This study confirms the involvement of these genes in CFS/ME.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular & Molecular Medicine, St George's University of London, London, UK.

ABSTRACT

Background: The authors have previously reported genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on expression of 88 human genes.

Aim: To attempt to reproduce these findings, determine the specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection.

Methods: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.

Results: In patients with CFS/ME, differential expression was confirmed for all 88 genes. Q-CFS/ME had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in patients with endogenous depression was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2 and PDCD6). Clustering of combined gene data in CFS/ME patients for this and the authors' previous study (117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus, enterovirus, Coxiella burnetii and parvovirus B19 revealed evidence of subtype-specific relationships for Epstein-Barr virus and enterovirus, the two most common infectious triggers of CFS/ME.

Conclusions: This study confirms the involvement of these genes in CFS/ME.

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Related in: MedlinePlus

Absolute fold-difference values (mean relative quantity (RQ) in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)/mean RQ in normal controls) for each of 88 CFS/ME-associated genes in eight CFS/ME subtypes (A–H).
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fig1: Absolute fold-difference values (mean relative quantity (RQ) in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)/mean RQ in normal controls) for each of 88 CFS/ME-associated genes in eight CFS/ME subtypes (A–H).

Mentions: Clustering of ΔCt values for the 88 CFS/ME-associated genes in the 117 CFS/ME patients identified eight subtypes (designated A–H), consisting of 27, 6, 19, 5, 21, 13, 19 and 4 CFS/ME patients, respectively. There were three patients whose gene profile did not fit into any of these eight subtype groupings. Mean fold-difference values for each CFS/ME subtype are shown in table 3 and figure 1. Most genes in each subtype were shown to be upregulated (figure 1 and table 3).


Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis.

Zhang L, Gough J, Christmas D, Mattey DL, Richards SC, Main J, Enlander D, Honeybourne D, Ayres JG, Nutt DJ, Kerr JR - J. Clin. Pathol. (2009)

Absolute fold-difference values (mean relative quantity (RQ) in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)/mean RQ in normal controls) for each of 88 CFS/ME-associated genes in eight CFS/ME subtypes (A–H).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC2921262&req=5

fig1: Absolute fold-difference values (mean relative quantity (RQ) in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)/mean RQ in normal controls) for each of 88 CFS/ME-associated genes in eight CFS/ME subtypes (A–H).
Mentions: Clustering of ΔCt values for the 88 CFS/ME-associated genes in the 117 CFS/ME patients identified eight subtypes (designated A–H), consisting of 27, 6, 19, 5, 21, 13, 19 and 4 CFS/ME patients, respectively. There were three patients whose gene profile did not fit into any of these eight subtype groupings. Mean fold-difference values for each CFS/ME subtype are shown in table 3 and figure 1. Most genes in each subtype were shown to be upregulated (figure 1 and table 3).

Bottom Line: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.In patients with CFS/ME, differential expression was confirmed for all 88 genes.This study confirms the involvement of these genes in CFS/ME.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular & Molecular Medicine, St George's University of London, London, UK.

ABSTRACT

Background: The authors have previously reported genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on expression of 88 human genes.

Aim: To attempt to reproduce these findings, determine the specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection.

Methods: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.

Results: In patients with CFS/ME, differential expression was confirmed for all 88 genes. Q-CFS/ME had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in patients with endogenous depression was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2 and PDCD6). Clustering of combined gene data in CFS/ME patients for this and the authors' previous study (117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus, enterovirus, Coxiella burnetii and parvovirus B19 revealed evidence of subtype-specific relationships for Epstein-Barr virus and enterovirus, the two most common infectious triggers of CFS/ME.

Conclusions: This study confirms the involvement of these genes in CFS/ME.

Show MeSH
Related in: MedlinePlus