J Clin Pathol doi:10.1136/jcp.2009.072561
  • Original article

Microbial infections in eight genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME)

Open Access
  1. Lihan Zhang1,
  2. John Goudh1,
  3. David Christmas2,
  4. Derek Mattey3,
  5. Selwyn Richards4,
  6. Janice Main5,
  7. Derek Enlander6,
  8. David Honeybourne7,
  9. Jon Ayres8,
  10. David J Nutt2,
  11. Jonathan Kerr1,*
  1. 1 St George's University of London, United Kingdom;
  2. 2 University of Bristol, United Kingdom;
  3. 3 Staffordshire Rheumatology Centre, United Kingdom;
  4. 4 Poole Hospital NHS Trust, United Kingdom;
  5. 5 Imperial College London, United Kingdom;
  6. 6 New York ME / CFS Service, United Kingdom;
  7. 7 Birmingham Heartlands Hospital, United Kingdom;
  8. 8 University of Birmingham, United Kingdom
  1. Correspondence to: Jonathan R Kerr, Dept of Cellular & Molecular Medicine, St George's University of London, Cranmer Terrace, London, SW17 0RE, United Kingdom; jkerr{at}
  • Received 5 October 2009
  • Accepted 3 November 2009
  • Published Online First 2 December 2009


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 CFS/ME (according to Fukuda criteria), 6 patients with Q-fever associated CFS/ME form the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous 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, 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.


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