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New Dr Kerr Gene Expression study published

Min

Messages
1,387
Location
UK
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."
 
K

Katie

Guest
I've been keeping a half eye on Dr Kerr's gene expression research since his pilot study years ago. It's exciting to read that their may well be distinct sub-types for EBV and enterovirus. It's also exciting to read further correlations between ME/CFS and certain genes and more research into slight tweak and changes depending on the trigger. Anything that furthers knowledge into our differences and similarities helps. Does this mean that if a genetic diagnostic test was formulated, that not only would you get a formal diagnosis but a type that told you what triggered your illness?


What I am most excited about is Dr Mikovits and Dr Kerr's grant to do ME/CFS pathophysiological research, it will be fascinating to see how XMRV might fit and possibly explain gene expression. Even if XMRV research falls through, this is positive research that should help a lot of us in the future. It's also good for those who (if XMRV does pan out) might test negative for XMRV that they might have a solid explanation from a genetic perspective. Am I right in thinking that this paper edges Dr Kerr another step further towards a diagnostic test? It's great to have another method of diagnosis on the horizon.
 

CBS

Senior Member
Messages
1,522
Another step closer

One more nail in the psychogenic theorist's coffin.

I'm glad he grouped patients from his original study with the new patients. The first study had such a small 'n' that the symptom categorization was likely to reveal only the most dramatic differences and some of those groupings were pretty shaky being based on as few as 2-4 patients. Some of the groups are still pretty small. I'm not surprised the groups' symptoms shifted a bit and wouldn't be surprised to see more shifting down the road.
 
C

cold_taste_of_tears

Guest
Thanks for this MIN its really interesting.

How sad that according to internet forums on CFS you can cure yourself with psychological therapies and we can be like them too if we weren't so blinkered. :cool:
Interesting they are never in need of any blood test to show they actually had a disease in the first place...

The clones of Psychiatry are in full force, but maybe someone will interupt their functioning soon with Science rather than psychobabble.
 

MEKoan

Senior Member
Messages
2,630
This is wonderful news!

Dr. Kerr has been on this trail, and giving us hope, for such a long time. I am delighted for us and for him that his research continues to bear such promising fruit!

It is good not to be completely dependent on the results of one study for validation of this illness. Dr. Kerr's gene work has been the most compelling work done thus far. The fact that he managed to do it in such a hostile environment is truly remarkable.

Thank you Dr. Kerr for carrying on with such difficult work!

The Kerr/Mikovitz team should be unstoppable.
 

kurt

Senior Member
Messages
1,186
Location
USA
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

Min,
Thanks for posting that. How interesting to see the dramatic subtype difference between US and UK cases of ME/CFS (see the tables at the end).
 
K

_Kim_

Guest
I'm in a bad crash today and having trouble reading this article, but there is one sentence that stands out in the discussion section. Depressed patients have different gene expression than CFS/ME patients.

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.
 

CBS

Senior Member
Messages
1,522
I'm in a bad crash today and having trouble reading this article, but there is one sentence that stands out in the discussion section. Depressed patients have different gene expression than CFS/ME patients.

Sorry about the bad day. Hopefully that one sentence will help.

Wish I was in Atlanta. I'd personally shellac it onto Bill Reeves office door and desk.
 

Kati

Patient in training
Messages
5,497
Wish I was in Atlanta. I'd personally shellac it onto Bill Reeves office door and desk.

We could all make a copy of the article and send it personnally to him? Wouldn't he like that? Or well, he may think we're a bunch of hystericals:rolleyes:
 
C

cold_taste_of_tears

Guest
Be careful you aren't ''medicalising'' your medical disease here.........

(((FLASHBACK))

*That would be very unfortunate you are openly 'focussing on physical symptoms'' and thus somatizing...........

*Remember it's your ''automatic negative thoughts'' that cause your illness....

*Please stop, and write down in your activity diary how many steps you have done today, to contribute towards your recovery plan. You do have a recovery plan don't you? Only patients who don't want to get better - don't have a plan of recovery.

(FLASHBACK))

Ohh it was all a dream it seems, we were crazy after all - no, wait...........
 

flybro

Senior Member
Messages
706
Location
pluto
Might we dance again?

IN YOUR FACE WEAS-LEY

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."
 

muffin

Senior Member
Messages
940
Good but more than $1.6 M is needed for CFIDS/

NIH Bets $1.6 Million on Continued ME/CFS Research by Drs. Mikovits & Kerr.

Yes this is great but we need far more than $1.6 Million.

What we need to do is to post the names/email addresses for ALL appropriate Congress people (Government Oversight, Federal Funding, etc) and hit them with emails on CFIDS research, XMRV research, and also investigations into the CDC/CFS/Reeves and his contracgtors - ABT Assoc. and Emory Uni MIND-BODY Program.
 
Messages
43
Location
Stockholm
Quotes from the study:


Expression of 88 human genes was confirmed as being significantly different between CFS/ME patients and normal controls.

Gene expression in endogenous depression patients was similar to that in the normal controls.

CFS/ME patients can be grouped into Genomic subtypes which have different clinical phenotypes.
 

Dolphin

Senior Member
Messages
17,567
There appears to be an error in this paper:

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).

According to the data in Table 2, PDCD2 is not upregulated but downregulated
in depression, the opposite of what happens in the CFS/ME group.

I mentioned this to Dr Kerr in an E-mail over the weekend (no reply as of yet).