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Dr. Jonathan Kerr's work
Microbial infections in eight genomic subtypes of Chronic Fatigue
Syndrome / Myalgic Encephalomyelitis (CFS/ME)
Lihan Zhang1,
John Goudh1, David Christmas2,
Derek Mattey3, Selwyn Richards4,
Janice Main5, Derek Enlander6,
David Honeybourne7, Jon Ayres8,
David J Nutt2, Jonathan Kerr1,*
1 St George's University of
London, United Kingdom;
2 University of Bristol, United Kingdom;
3 Staffordshire Rheumatology Centre, United Kingdom;
4 Poole Hospital NHS Trust, United Kingdom;
5 Imperial College London, United Kingdom;
6 New York ME / CFS Service, United Kingdom;
7 Birmingham Heartlands Hospital, United Kingdom;
8 University of Birmingham, United Kingdom
Correspondence to: Jonathan R Kerr, Dept of Cellular &
Molecular Medicine, St George's University of London, Cranmer Terrace, London,
SW17 0RE, United Kingdom;
jkerr@sgul.ac.uk
Accepted November 3, 2009 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 subtype-specific relationships for EBV and
enterovirus, the two most common infectious triggers of CFS/ME.
http://jcp.bmj.com/content/early/2009/11/26/jcp.2009.072561.abstract

Jonathan R. Kerr1,7,
John Gough1, Selwyn C. M. Richards2,
Janice Main3, Derek Enlander4,
Michelle McCreary5, Anthony L. Komaroff5
and John K. Chia61
St George's University of London;
2 Poole Hospital NHS Trust;
3 Imperial College London;
4 New York ME/CFS Service;
5 Brigham & Women's Hospital, Harvard Medical School;
6 ID Med, Torrance, CA
Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME)
is a neuro-immune disease of uncertain pathogenesis. Human parvovirus
B19 infection has been shown to occur just prior to development
of the onset of CFS/ME in several cases, although B19 seroprevalence
studies do not shown any significant differences between CFS/ME and
controls.
In this study, we analysed parvovirus B19 markers in CFS/ME
patients (n=200), diagnosed according to Fukuda CDC criteria, and
normal blood donors (n=200). Serum from each subject was tested for
anti-B19 VP2 IgM and IgG (by Biotrin ELISA), anti-B19 NS1 IgM and IgG
(by immunoflourescence), and B19 DNA by real-time PCR. CFS/ME
patients and normal blood donors had a similar B19 seroprevalence
(75% versus 78%, respectively).
Eighty-three CFS patients (41.5%) as
compared with fourteen (7%) of normal blood donors tested positive
for anti-B19 NS1 IgG ( 2=
64.8; P<0.0001; Odds ratio = 9.42, CI 5.11 – 17.38). Of these 83
patients, 61 complained of chronic joint pain, while 22 did not.
Parvovirus B19 DNA was detected in serum of 11 CFS patients and none
of the controls by Taqman real-time PCR ( 2
= 9.35, P<0.002. Positivity for anti-B19 NS1 IgG was associated with
higher expression levels of the human CFS-associated genes NHLH1 and
GABPA.
As NS1 antibodies are thought to indicate chronic or severe
courses of B19 infection, these findings suggest that although the
seroprevalence of B19 in CFS patients is similar to controls, the
immune control of the virus may not be efficient.
Full text -
http://vir.sgmjournals.org/cgi/content/abstract/vir.0.017590-0v1

Dr Jonathan Kerr of Imperial College London, supported by the CFSRF,
published a paper containing early results in the
Journal of
Clinical Pathology (J Clin Path 2005; 8:860-863, pdf format) in August 2005.
Fifteen genes were discovered to be up to 4 times as active in ME sufferers
compared with a control group. Dr. Kerr is continuing his studies using a larger
group of patients.
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