Re: Dr. Kerr's work

March 2, 2006

I was thinking it might be that drug too. I see it went into Phase 11 clinical

development program for the treatment of CFS in the US in late October and

wondered about it at the time.

bf

From: H. Wish

Sent: Thursday, March 02, 2006 10:48 AM

Subject: Dr. Kerr's work

I'm guessing it is isoprinosine - anyone know?

>Hi All, here is an article from the Telegraph newspaper in the UK on

>the latest on Dr Kerr's gene expression workwork. I was going to copy

>it directly but then I read their statment about copyright so thought

>I'd better not to! Is that being too cautious?

>

>It says that there is a drug, already existing, that potentially could

> be used to treat CFS.

This list is intended for patients to share personal experiences with each

other, not to give medical advice. If you are interested in any treatment

discussed here, please consult your doctor.

March 2, 2006

Well if it is don't expect any miracles - been there done that didn't

work

Rosie

Subject: Dr. Kerr's work

I'm guessing it is isoprinosine - anyone know?

>Hi All, here is an article from the Telegraph newspaper in the UK on

>the latest on Dr Kerr's gene expression workwork. I was going to copy

>it directly but then I read their statment about copyright so thought

>I'd better not to! Is that being too cautious?

>

>It says that there is a drug, already existing, that potentially could

> be used to treat CFS.

This list is intended for patients to share personal experiences with

each other, not to give medical advice. If you are interested in any

treatment discussed here, please consult your doctor.

March 2, 2006

I have good reason to believe it isn't Isoprinosine (as Newport

Pharmaceuticals asked me what the drug was when I had the appended letter

published in the Irish Medical Times very recently and I presume they'd

know!). Don't know what it is (a couple of these paragraphs are from

something Dr. Kerr sent us).

Tom

http://www.imt.ie/disLetter.asp?WID=220 & LID=717

Talk on chronic fatigue syndrome research

Dear Editor,

The article, " Chronic fatigue syndrome caused by many factors " in Clinical

World (Irish Medical Times 10/2/2006) was a summary of a review by a Dutch

team who deal with patients with various fatigue states include Chronic

Fatigue Syndrome (CFS).

Readers might be interested to know that there is much disagreement within

the research world about what causes CFS and how it should be treated, and

many researchers would prioritise other areas.

One such researcher is Dr Kerr BSc, MBBCh, MD, PhD, FRCPath, Sir

ph Hotung Clinical Senior Lecturer in Inflammation in St 's

University of London. Dr Kerr (a graduate of Queen's University, Belfast)

will be giving talks on his research into CFS in Dublin and Waterford on May

6 and 7 respectively this year.

His interest in CFS began during a study of the consequences of parvo-virus

B19 infection, when he showed that a percentage of infected cases developed

CFS which persisted for several years. He is now the principal investigator

in a programme of research in CFS.

This involves development of a diagnostic test using mass spectrometry,

analysis of human and viral gene expression in the white blood cells, and

clinical trials of immunomodulatory drugs. He has previously published

research showing, amongst other things, the clinical benefit of using

intravenous Immunoglobulin Therapy in Parvovirus B19-Associated Chronic

Fatigue Syndrome (Clin Infect Dis. 36: e100-e106).

Dr Kerr is funded by the CFS Research Foundation. The Irish ME/CFS Support

Group has given 28,000 to the CFS Research Foundation in recent years and

hopes to give more in the future to help support cutting-edge research

projects such as those currently being led by Dr Kerr.

If anyone would like further information on the talks Dr Kerr is giving, or

information on his research or other research in the field, please do not

hesitate to contact us.

Tom Kindlon,

Assistant Chairperson

Irish ME/CFS Support Group,

PO Box 3075, Dublin 2.

March 2, 2006

Hi Tom,

Thanks for that info, I was thinking it wouldn't be isoprinosine or

kutapressin or any of the drugs quite a few people have tried

experimentally, that are the obvious ones we think of when we hear

'immunomodulatory'.

Surely it wouldn't be too hard for someone who understand how these

things work to make an educated guess? Hoping someone here can do

that. How I miss 's contributions at times like this, he would

have come up with something.

I did a couple of googles on some of the dysfunctional genes plus the

word 'immunomodulatory' but it's all a bit above my head.

>

> I have good reason to believe it isn't Isoprinosine (as Newport

> Pharmaceuticals asked me what the drug was when I had the appended

letter

> published in the Irish Medical Times very recently and I presume they'd

> know!). Don't know what it is (a couple of these paragraphs are from

> something Dr. Kerr sent us).

>

> Tom

>

> http://www.imt.ie/disLetter.asp?WID=220 & LID=717

>

> Talk on chronic fatigue syndrome research

>

> Dear Editor,

>

> The article, " Chronic fatigue syndrome caused by many factors " in

Clinical

> World (Irish Medical Times 10/2/2006) was a summary of a review by a

Dutch

> team who deal with patients with various fatigue states include Chronic

> Fatigue Syndrome (CFS).

> Readers might be interested to know that there is much disagreement

within

> the research world about what causes CFS and how it should be

treated, and

> many researchers would prioritise other areas.

>

> One such researcher is Dr Kerr BSc, MBBCh, MD, PhD,

FRCPath, Sir

> ph Hotung Clinical Senior Lecturer in Inflammation in St 's

> University of London. Dr Kerr (a graduate of Queen's University,

Belfast)

> will be giving talks on his research into CFS in Dublin and

Waterford on May

> 6 and 7 respectively this year.

>

> His interest in CFS began during a study of the consequences of

parvo-virus

> B19 infection, when he showed that a percentage of infected cases

developed

> CFS which persisted for several years. He is now the principal

investigator

> in a programme of research in CFS.

>

> This involves development of a diagnostic test using mass spectrometry,

> analysis of human and viral gene expression in the white blood

cells, and

> clinical trials of immunomodulatory drugs. He has previously published

> research showing, amongst other things, the clinical benefit of using

> intravenous Immunoglobulin Therapy in Parvovirus B19-Associated Chronic

> Fatigue Syndrome (Clin Infect Dis. 36: e100-e106).

>

> Dr Kerr is funded by the CFS Research Foundation. The Irish ME/CFS

Support

> Group has given 28,000 to the CFS Research Foundation in recent

years and

> hopes to give more in the future to help support cutting-edge research

> projects such as those currently being led by Dr Kerr.

>

> If anyone would like further information on the talks Dr Kerr is

giving, or

> information on his research or other research in the field, please

do not

> hesitate to contact us.

>

> Tom Kindlon,

> Assistant Chairperson

> Irish ME/CFS Support Group,

> PO Box 3075, Dublin 2.

>

March 2, 2006

Ive heard more about Gows findings myself - unsure about Kerrs.

However, if significantly activated macrophages are the major feature

(as I think Gow has found), this would suggest CFS is an inflammatory

disease.

Because, of course, no persisting microbe has been agreed to be the

cause of CFS, it would then probably be treated as an autoimmune

disease like lupus, MS, and RA. No one has actually shown how

most " autoimmune " diseases are caused by autoimmunity, and they may

or may not be; even the scientists who casually refer to these

diseases being autoimmune admit that hard proof is yet to come. They

might be autoimmune, there may be some vague " mix " of autoimmunity

and chronic infection - or there may be a drastic overreaction to a

chronic infection.

Whatever it is, the outcome is inflammation, ie activation of the

immune system. And I think the drugs theyl be examining are

immunosuppressive ones. Things like steroids (eg prednisone),

remicade (anti-TNFa antibody), MTX, cyclosporin, rituximab. Whether

these treatments are a good idea, is a question I dont know much

about. I'm not sure whether controlled trials have been performed to

see whether these treatments actually help lupus/RA/etc patients in

the long term. They certainly do have an effect on those diseases in

the short term.

The Chia treatment that has kindly updated us on in #92205,

is like, the diametric opposite approach. Hes using INF-a and IFN-g

to *intensify* the immune activation. Many chronically-infective

organisms interfere with your immune systems function. They might

throw a wrench in the works to prevent immunity from fully activating

and killing the infection. Injecting INF could overcome this impasse.

This is the simplest, and probably the most plausible, way to explain

a benefit from INF treatment. I suppose its also conceivable that INF

could downregulate immunity in some sort of paradoxical way. I dont

know of a relevant precedent for that - but please note I dont know

anything about INFa. I do know that IFNg favors greater activation of

immunity in every context I have ever heard of.

So, to really flesh out the map of different theories here, you have

some viewpoints where the whole inflammation / immune activation

aspect is not the sole focus. For example, Rich focuses on metabolic

breakdowns like loss of reduced glutathione, and argues that the

inflammation could be due to the immune systems inability to fight

off microbes when reduced glutathione status is poor.

But personally, I do think the immune activation is the center of the

problem. And I tend more towards Chias side; I tend to think there

are persisting microbes figuring in most inflammatory diseases. There

isnt proof but theres suggestive evidence. Chia likes a viral cause

for CFS; I am personally more interested in bacteria, but am fairly

ignorant of viruses and of Chias evidence.

Suppressing your immune system is probably a pretty good thing if

your immune system is just reacting to your own body. But it could be

a bad thing if you have some sort of chronic infection. Or not: if

the immune suppression doesnt cause the infection to grow, it would

make you feel better without being harmful - but I dont think theres

very much precedent for such a thing occuring. That doesnt mean it

cant happen. But speculation cant really decide these things; only

data can.

I personally have had terrific luck with antibacterials.

>

> Hi Tom,

>

> Thanks for that info, I was thinking it wouldn't be isoprinosine or

> kutapressin or any of the drugs quite a few people have tried

> experimentally, that are the obvious ones we think of when we hear

> 'immunomodulatory'.

>

> Surely it wouldn't be too hard for someone who understand how these

> things work to make an educated guess? Hoping someone here can do

> that. How I miss 's contributions at times like this, he would

> have come up with something.

>

> I did a couple of googles on some of the dysfunctional genes plus

the

> word 'immunomodulatory' but it's all a bit above my head.

>

March 3, 2006

Hi ,

First of all, I want to say there's a lot of excellent points in your

post and I agree with much of it. However, I don't see any reason to

assume Kerr is thinking of immunosuppressive drugs... would he not

have said that rather than immunomodulatory, if that were the case?

You mentioned interferon... even this is classed as immunomodulatory -

we don't really know which way he's going to go. I'd think if someone

could work out which drugs affect the genes mentioned in his papers,

we might be closer to having an idea.

I personally don't think, given the quality of his research, that he'd

be confident about a treatment possibility if it were something as

ordinary as steroids etc.

Also, I haven't had any luck with antibiotics myself, so favour a

viral causation. I do agree there are possibly persistent infections,

and maybe they are bacterial for some, viral for others (or both). I

do think that a lot of us must have a persistent virus or a viral

trigger that caused immune system changes and that the reason

treatment is so elusive is that viruses are harder to treat, and many

aren't understood yet.

> >

> > Hi Tom,

> >

> > Thanks for that info, I was thinking it wouldn't be isoprinosine or

> > kutapressin or any of the drugs quite a few people have tried

> > experimentally, that are the obvious ones we think of when we hear

> > 'immunomodulatory'.

> >

> > Surely it wouldn't be too hard for someone who understand how these

> > things work to make an educated guess? Hoping someone here can do

> > that. How I miss 's contributions at times like this, he would

> > have come up with something.

> >

> > I did a couple of googles on some of the dysfunctional genes plus

> the

> > word 'immunomodulatory' but it's all a bit above my head.

> >

>

March 3, 2006

,

Which have you used with success?

Thanks,

Ellen

>

> I personally have had terrific luck with antibacterials.

>

March 3, 2006

thanks for that great summary! I just want to note that IFN-a has been shown to

return perforin deficient AIDS and hepatitis C patients to normal NK cell

functioning - and we've recently seen that CFS patients are perforin deficient -

probably, the authors t hought, because of an ongoing immune response. This

type of response has been shown to occur in AIDS. The authors didnt state what

they thought the pathogen(s) were in CFS.

Cort

<usenethod@...> wrote: