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2009
 Microbial
infections in eight genomic subtypes of Chronic Fatigue Syndrome
/ Myalgic Encephalomyelitis (CFS/ME) Lihan Zhang,
John Goudh, David Christmas, Derek Mattey, Selwyn Richards,
Janice Main, Derek Enlander, David Honeybourne, Jon Ayres, David
J Nutt and Jonathan Kerr. "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."
2007
Seven
genomic subtypes of Chronic Fatigue Syndrome / Myalgic
Encephalomyelitis (CFS/ME): a detailed analysis of gene networks
and clinical phenotypes. Jonathan Kerr, Beverly Burke,
Robert Petty, John Gough, David Fear, Mattey David, John Axford,
Angus Dalgleish and David Nutt. "...we report in detail
the genomic and phenotypic differences in 7 genomically-defined
subtypes of CFS."
Text only version
2006
A
first study of cytokine genomic polymorphisms in CFS: Positive
association of TNF-857 and IFNgamma 874 rare alleles.
(Abstract) N. Carlo-Stella, C. Badulli, A. De Silvestri, L.
Bazzichi, M. Martinetti, L. Lorusso, S. Bombardieri, L.Salvaneschi,
M. Cuccia; Affiliations: University of Pavia, San Matteo
Polyclinic Hospital, Pavia; S. Chiara Hospital, Pisa; M. Mellini
Hospital, Chiari, (BS), Italy. "We hypothesize that CFS
patients can have a genetic predisposition to an immunomodulatory
response of an inflammatory nature probably secondary to one or
more environmental insults of unknown nature."
Preliminary
evidence of mitochondrial dysfunction associated with
post-infective fatigue after acute infection with Epstein Barr
Virus. Suzanne D Vernon, Toni Whistler, Barbara
Cameron, Ian B Hickie, William C Reeves and Andrew Lloyd; Centers
for Disease Control and Prevention, USA, University of New South
Wales, Sydney "A small proportion of people that develop
infectious mononucleosis following EBV infection remain sick with
chronic fatigue syndrome. Gene expression profiling was used to
determine whether failure to recover reflected altered gene
expression. The subjects who did not recover from infectious
mononucleosis had altered gene expression response during the
early phase of EBV infection compared to those who subsequently
recovered uneventfully. There were several differentially
expressed genes identified including gene involved in the immune
response, apoptosis and the cell cycle. A comparison of gene
expression profiles early and late following EBV infection
revealed that those who did not recover had differentially
expressed genes implicating mitochondrial perturbations with fatty
acid metabolism, mitochondrial function and apoptosis pathways."
2005
Gene
expression in peripheral blood mononuclear cells from patients
with chronic fatigue syndrome. N Kaushik, D Fear,
S C M Richards, C R McDermott, E F Nuwaysir, P Kellam, T J
Harrison, R J Wilkinson, D A J Tyrrell, S T Holgate and J R Kerr
(UK) "We report the differential expression of 16 human genes
in patients with CFS compared with normal controls. The
involvement of genes from several disparate pathways suggests a
complex pathogenesis involving T cell activation and abnormalities
of neuronal and mitochondrial function, and suggests possible
molecular bases for the recognised contributions of
organophosphate exposure and virus infection, respectively."
(Absract
only)
Whole-Genome
(33,000 genes) Affymetrix DNA Microarray Analysis of Gene
Expression in Chronic Fatigue Syndrome. (Abstract)
Gow JW, Cannon C, Behan WMH, Herzyk P, Keir S,
Riboldi-Tunnicliffe G, Behan PO & Chaudhuri A.; University of
Glasgow Department of Neurology, Southern General Hospital,
Scotland, UK "Findings:
Iterative group analysis of the differentially expressed genes
indicate that in CFS:
(a) there is a shift of immune response with preferential antigen
presentation to MHC class II receptors, downregulation of the MHC
class I system with a consequential suppression of Natural Killer
cells and fÑT-cell receptors, (b) increased cell membrane
prostaglandin-endoperoxide synthase activity with downstream
changes in oxygen transport and (c) macrophage activation with
phagocytosis of apoptotic neutrophils. Western blot/ELISA
assays of key biomarker genes can be used to support the clinical
diagnosis and identify candidates for treatment trials in CFS."
2003
Identification
of novel expressed sequences, up-regulated in the leucocytes of
chronic fatigue syndrome patients. R. Powell J.
Ren, G. Lewith, W. Barclay, S. Holgate and J. Almond; Southampton
University Hospital, Southhampton, UK, Reading University,
Reading, UK, and Aventis, Strasbourg, France "Twelve short
expressed sequence tags have been identified that were
over-expressed in lymphocytes from CFS patients. Although
differential display was the leading technology at the start of
this project, this is no longer the case. Gene chip technologies
offer a more thorough way of analysing changes in gene expression
and the most natural progression of this study would be the
application of these techniques to CFS. This preliminary
study shows that such an approach is well justified and predicts
that a more detailed characterization would identify more
candidate genes for this disease."
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