CFS et al...

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Found this while scurrying about looking for other stuff.

It was hiding in a professional health group I am in. Hope it is interesting.

Kaushik N, Fear D, s

SCM, et al. Gene expression in peripheral blood mononuclear cells from patients

with chronic fatigue syndrome.

J Clin Path 2005;58:826-832.

Narendra Kaushik,

Fear, Selwyn CM s, Clare R McDermott, Emile F Nuwaysir, Kellam, Tim

J on, J Wilkinson, AJ Tyrrell, T Holgate, R

Kerr Fritz E, J, Kerr JR, et al. Association of chronic fatigue syndrome

with human leukocyte antigen class ii alleles. Clin Path 2005;58:860-863.

Chronic fatigue is not all in the mind

21 July 2005

NewScientist.com news

service

Rowan Hooper

AT LONG last, we are

beginning to get to grips with chronic fatigue syndrome. Differences in gene

expression have been found in the immune cells of people with the disease, a

discovery that could lead to a blood test for the disorder and perhaps even to

drugs for treating it.

The symptoms of chronic

fatigue syndrome have been compared to those of a really bad hangover: extreme

weakness, inability to think straight, disrupted sleep and headache. But unlike

a hangover, the symptoms linger for years, devastating people's lives.

While nobody doubts CFS

exists, just about every aspect of it is controversial. Some say it is the same

as myalgic encephalomyelitis, or ME; others disagree. Many specialists are

convinced it does have a biological basis, but pinning down physical abnormalities

common to all patients has proved tough. People with CFS have often received

little sympathy from doctors who dismiss it as " all in the mind " .

Now Kerr's team,

which is moving to St 's University of London,

has compared levels of gene expression in the white blood cells of 25 healthy

individuals with those in 25 patients diagnosed as having CFS according to

strict criteria. The researchers found differences in 35 of the 9522 genes they

analysed using DNA chip technology.

The few similar studies done

in the past have produced conflicting results, so the team double-checked their

results using a more accurate method called real-time PCR. That confirmed that

15 of the genes were up to four times as active in people with CFS, while one gene

was less active. The results will appear in the Journal of Clinical Pathology

next month.

Kerr is repeating the study

in 1000 CFS patients and healthy controls, this time looking at 47,000 gene

products. So far, the larger study backs up the earlier results, he told New

Scientist.

If Kerr really has succeeded

where many have failed, and identified clear physical changes in people with

CFS, the lingering opinion that it is " all in the mind " could finally

be laid to rest. " This exciting new work shows that some aspects of this

complex illness may be understandable in molecular terms, and that CFS is not a

'made up'

illness, " says Lane, a

neurologist at Charing Cross Hospital in London.

It should also be possible

to develop a blood test for CFS. The team has already discovered differences in

blood proteins related to the changes in gene expression.

Kerr hopes the work might

even lead to treatments. " We have shown that a significant part of the

pathogenesis resides in the white blood cells and in their activity, " he

says. " It will open the door to development of pharmacological

interventions. "

Several of the genes

identified by the team in CFS play important roles in mitochondria, the power

factories of our cells. " The involvement of such genes does seem to fit

with the fact that these patients lack energy and suffer from fatigue, "

Kerr says.

One of these gene products,

EIF4G1, is involved in protein production in mitochondria. It is hijacked by

some viruses, so cells may compensate by ramping up gene expression. " I am

excited by the paper, " says Basant Puri, a CFS expert at Hammersmith Hospital

in London.

" The group's finding of upregulation of EIF4G1 is consistent with

subclinical persistent viral infection. "

This fits in with the idea

that CFS is sometimes triggered by viruses such as Epstein-Barr, Q fever,

enteroviruses and parvovirus B19. " CFS often begins with a flu-like

illness which never goes away, " Kerr says.

Of the other genes whose

expression varies in CFS patients, some are involved in regulating the activity

of the immune system. Others play important roles in nerve cells, including a

gene called NTE, which codes for an enzyme affected by organophosphates and

nerve gases.

Journal reference: Journal of Clinical Pathology

(vol 58, p 823, 860) From issue 2509 of New Scientist magazine, 21 July 2005,

page 9 http://www.newscientist.com/article.ns?id=mg18725093.700

Bruce Guilmette, Ph.D.

Survive Cancer Foundation, Inc.

http://www.survivecancer.net