New Dr Kerr Gene Expression study published: http://jcp.bmj.com/cgi/rapidpdf/jcp.2009.072561v1 http://jcp.bmj.com/cgi/content/short/jcp.2009.072561v1?rss=1 'Microbial infections in eight genomic subtypes of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)' JCP Online First, published on December 2, 2009 as 10.1136/jcp.2009.072561 Abstract 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 evidence of subtype-specific relationships for EBV and enterovirus, the two most common infectious triggers of CFS/ME. Keywords: Chronic fatigue syndrome, myalgic encephalomyelitis, subtypes, gene expression, endogenous depression, Epstein-Barr virus, parvovirus B19, Coxiella burnetii, enterovirus Lihan Zhang,1 John Gough,1 David Christmas,2 Derek L Mattey,3 Selwyn CM Richards,4 Janice Main, 5 Derek Enlander,6 David Honeybourne,7 Jon G Ayres,8 David J Nutt,2 Jonathan R Kerr.1 1Department of Cellular & Molecular Medicine, St George's University of London, London, UK; 2Psychopharmacology Unit, Dept of Community Based Medicine, University of Bristol, Bristol, UK; 3Staffordshire Rheumatology Centre, Stoke on Trent, UK; 4Dorset CFS Service, Poole Hospital, Dorset, UK; 5Dept of Infectious Diseases and General Medicine, Imperial College London, St Mary's Hospital, London, UK; 6New York ME / CFS Service, 860 Fifth Avenue, New York, USA; 7Dept of Respiratory Medicine, Birmingham Heartlands Hospital, UK; 8Dept of Environmental and Occupational Medicine, University of Birmingham, UK. JCP Online First, published on December 2, 2009 as 10.1136/jcp.2009.072561 & from the discussion section: "The fact that only 5 of these genes were abnormally expressed in endogenous depression patients as compared with normals, supports the view that CFS/ME and endogenous depression are biologically distinct, and that the psychological features of CFS/ME are in fact secondary to the pathogenesis."