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Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis
  1. Lihan Zhang1,
  2. John Gough1,
  3. David Christmas2,
  4. Derek L Mattey3,
  5. Selwyn C M Richards4,
  6. Janice Main5,
  7. Derek Enlander6,
  8. David Honeybourne7,
  9. Jon G Ayres8,
  10. David J Nutt2,
  11. Jonathan R Kerr1
  1. 1Department of Cellular & Molecular Medicine, St George's University of London, London, UK
  2. 2Psychopharmacology Unit, Department of Community Based Medicine, University of Bristol, Bristol, UK
  3. 3Staffordshire Rheumatology Centre, Stoke on Trent, UK
  4. 4Dorset CFS Service, Poole Hospital, Dorset, UK
  5. 5Department of Infectious Diseases and General Medicine, Imperial College London, St Mary's Hospital, London, UK
  6. 6New York ME/CFS Service, New York, USA
  7. 7Department of Respiratory Medicine, Birmingham Heartlands Hospital, Birmingham, UK
  8. 8Department of Environmental and Occupational Medicine, University of Birmingham, Birmingham, UK
  1. Correspondence to Dr Jonathan R Kerr, Room 2.267, Jenner Wing, St George's University of London, Cranmer Terrace, London SW17 0RE, UK; jkerr{at}sgul.ac.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.

  • Chronic fatigue syndrome
  • myalgic encephalomyelitis
  • subtypes
  • gene expression
  • endogenous depression
  • Epstein–Barr virus
  • parvovirus B19
  • Coxiella burnetii
  • enterovirus
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Footnotes

  • This work was presented at the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFSME), Reno, Nevada, USA, March 2009.

  • Funding Wellcome Trust; CFS Research Foundation.

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the Wandsworth Research Ethics Committee, St George's Hospital.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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