Re: Lower frequency of IL-17F sequence variant (His161Arg) in chronic fatigue sy

[Guest guest]

Hey, nice find... I don't have it to read or I would... hopefully,

this will be independently confirmed ASAP.

Private genome sequencing is now available for US$350,000, and the

firm doing it has at least 20 'nomes on order so far. Poking through

secondary/popular information only, I haven't seen much dissent from

the view that it will soon be down more towards the range of US$1,000,

maybe in five years. Today's opinion is no guarantee, but it may

actually happen.

Perhaps this will alter CFS politics rapidly, assuming there is

something to find in the genome, which seems likely.

Now, I don't know too much about genome scanning -- only know what I

hear, not actual data. But I know the current techniques using SNPs

(and formerly microsatellites) are not so shabby. However, I heard it

said that copy number variations (CNVs) are something that haven't

been too fully explored by the genome scans that have been used so

far. So I think(?) it seems that a lot of people are still expecting

new genetic factors to probably be uncovered in future, even in the

well-scanned phenotypes such as lupus. CFS hasn't ever been scanned in

the first place as far as I know (though I would expect MHC

associations have probably been looked for).

Another issue to be aware of in disease genetics, are the " rare

variants " and " common variants " hypotheses of common diseases.

Basically there are some who think that genetic variants that are

factors in common diseases are going to mostly be common ones, and

others who expect them to mostly be rare ones. In truth, to the best

of my knowledge, there aren't a hell of a lot of strong reasons to

expect that there won't be a complete range from common to rare.

Anyway, the ones discovered so far are common, because they are easier

to discover without having immense numbers of fully-sequenced genomes,

which of course we don't have so far.

Of course, these genetic factors don't have to be the complete causes

of the diseases, and almost certainly won't be. Even the portion of

contribution to disease genesis that they do make, need not be

unmixedly genetic; it could be most of these factors don't contribute

anything much to disease genesis (or anything at all) without the

presence of certain environmental factors with which they interact.

> *Biochemical and Biophysical Researche Communications*. 2008 Sep 4.

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> *Lower frequency of IL-17F sequence variant (His161Arg) in chronic

fatigue

> syndrome patients.*

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> Metzger K, Frémont M, Roelant C, De Meirleir K.

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> Protea Biopharma, Z.1-Researchpark 100, 1731 Zellik, Belgium.

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> Chronic fatigue syndrome (CFS) is characterized by immune dysfunctions

> including chronic immune activation, inflammation, and alteration of

> cytokine profiles. T helper 17 (Th17) cells belong to a recently

identified

> subset of T helper cells, with crucial regulatory function in

inflammatory

> and autoimmune processes. Th17 cells are implicated in allergic

> inflammation, intestinal diseases, central nervous system inflammation,

> disorders that may all contribute to the pathophysiology of CFS.

IL-17F is

> one of the pro-inflammatory cytokines secreted by Th17 cells. We

> investigated the association between CFS and the frequency of

rs763780, a

> C/T genetic polymorphism leading to His161Arg substitution in the IL-17F

> protein. The His161Arg variant (C allele) antagonizes the

pro-inflammatory

> effects of the wild-type IL-17F. A significantly lower frequency of

the C

> allele was observed in the CFS population, suggesting that the His161Arg

> variant may confer protection against the disease. These results

suggest a

> role of Th17 cells in the pathogenesis of CFS.

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> PMID: 18774769 [PubMed - as supplied by publisher]

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> Source from url:

http://www.ncbi.nlm.nih.gov/pubmed/18774769?dopt=Abstract

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> <http://www.ncbi.nlm.nih.gov/pubmed/18774769?dopt=Abstract>

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