Journal of IiME Volume 3 Issue 1 www.investinme.org P PRROOFFIILLEESS ooff PPRREESSEENNTTEERRSS aatt tthhee IINNVVEESSTT iinn MMEE I INNTTEERRNNAATTIIOONNAALL MMEE//CCFFSS CCOONNFFEERREENNCCEE The study, and its results, raises some important questions. The first of which pertains to the need for funding of microbiological CFS research. He is funded (>£1million) by the CFS Research Foundation (www.cfsrf.com), a charitable organization based in the U.K., and leads a group of 5 scientists at St George's. The Foundation needs private support to continue their research efforts. They also openly post the results of their efforts on their website http://www.cfsrf.com. C Coonnffeerreennccee PPrreesseennttaatt iioonn :: Microbial infections in eight genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME) Lihan Zhang,1 Beverley Burke,1* Robert Petty,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,7 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, Birminghan Heartlands Hospital, UK Reprints or correspondence: Dr Jonathan R Kerr, Room 2.267, Jenner Wing, St George’s University of London, Cranmer Terrace, London SW17 0RE, UK. Email: jkerr@sgul.ac.uk. Abstract Jonathan Kerr We have previously reported abnormal expression of 88 human genes in the blood of patients with Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME) and 7 genomic subtypes of CFS/ME (Kerr JR, et al. J Infect Dis 2008;197:1171-84). In this study we attempted to reproduce our previous findings in 59 new CFS patients, to determine expression levels of these genes in patients with endogenous depression, and to test the hypothesis that particular microbial infections are associated with particular genomic CFS subtypes. We determined expression levels of 88 human genes in blood of 53 new patients with idiopathic CFS/ME (according to Fukuda criteria), 6 patients with Q-fever associated CFS/ME (Q-CFS/ME) from 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 in the case of four genes (APP, GNAS, PDCD2, PDCD6), where significant upregulation (fold-difference ≥1.5) was noted. Taqman PCR delta Ct values for 88 genes in CFS/ME patients in the present study (n=59) and our previous study (n=55) were combined resulting in a gene database of 117 CFS/ME patients. Clustering revealed 8 genomic subtypes with distinct differences in SF-36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus (EBV), enterovirus, Chlamydia pneumoniae, Coxiella burnetii and parvovirus B19 revealed significant subtype-specific relationships for EBV and enterovirus, the two most common infectious triggers of CFS/ME. Invest in ME (Charity Nr. 1114035) Page 66/76
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