Gene Expression Subtypes in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis.
Journal: J Infect Dis. 2008 Apr 15;197(8):1171-1184.
Authors: Kerr JR, Petty R, Burke B, Gough J, Fear D, Sinclair LI,
Mattey DL, Richards SC, Montgomery J, Baldwin DA, Kellam P, Harrison
TJ, Griffin GE, Main J, Enlander D, Nutt DJ, Holgate ST.
Affiliations:
Department of Cellular & Molecular Medicine, St. George's University
of London,
Department of Asthma, Allergy and Respiratory Sciences, King's College London,
Departments of Infection and Medicine, Windeyer Institute of Medical
Sciences, University College London,
and Department of Infectious Diseases and General Medicine, Imperial
College London, St. Mary's Hospital, London,
Psychopharmacology Unit, Department of Community Based Medicine,
University of Bristol, Bristol,
Staffordshire Rheumatology Centre, Stoke on Trent, 8Dorset CFS
Service, Poole Hospital, Dorset, and
MRC Department of Immunopharmacology, University of Southampton,
Southampton General Hospital, Southampton, United Kingdom;
Penn Microarray Facility, University of Pennsylvania, Philadelphia; and
New York ME/CFS Service, New York, New York.
NLM Citation: PMID: 18462164
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a
multisystem disease, the pathogenesis of which remains undetermined.
We set out to determine the precise abnormalities of gene expression
in the blood of patients with CFS/ME. We analyzed gene expression in
peripheral blood from 25 patients with CFS/ME diagnosed according to
the Centers for Disease Control and Prevention diagnostic criteria
and 50 healthy blood donors, using a microarray with a cutoff fold
difference of expression of >/=2.5. Genes showing differential
expression were further analyzed in 55 patients with CFS/ME and 75
healthy blood donors, using quantitative polymerase chain reaction.
Differential expression was confirmed for 88 genes; 85 were
upregulated, and 3 were downregulated. Highly represented functions
were hematological disease and function, immunological disease and
function, cancer, cell death, immune response, and infection.
Clustering of quantitative polymerase chain reaction data from
patients with CFS/ME revealed 7 subtypes with distinct differences in
Medical Outcomes Survey Short Form-36 scores, clinical phenotypes,
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