Is anyone else wondering about this besides me? Anyone care to take a stab at answering this?
In the GD-MCB hypothesis that I've proposed to explain the pathogenesis of CFS involving a partial methylation cycle block, the things that are necessary to bring this about and cause the onset of a case of CFS are the following:
1. A genetic predisposition involving a combination of polymorphisms that have been inherited. Which polymorphisms are necessary has not yet been well-defined, and we need more research in this area. But various lines of evidence lead to the conclusion that there is a genetic component, though it is not yet thoroughly deliniated by research.
2. Exposure to a stressor or a set of stressors that place demands on glutathione and lower it sufficiently to leave vitamin B12 unprotected, setting up a partial block in the methylation cycle. There is a variety of stressors that can contribute to this, including physical, chemical, biological and psychological/emotional stressors, and in many cases I've studied, several of these have impacted the person simultaneously, as in a "perfect storm."
Getting to your question, while I don't know a lot about XMRV yet, I think there are a couple of ways it could figure into this picture. First, since it integrates itself into the human genome, I think it could have a somewhat similar effect as an inherited polymorphism. That is, it could affect the expression of the genes.
Second, I think another possibility would be that it could help to lower the glutathione level, either by a genetic effect on the enzymes that synthesize glutathione, or by a biochemical effect, such as by depleting cysteine, which is the rate-limiting amino acid for making glutathione, or by an immune system effect, such as by depleting glutathione when it deals with the oxidative stress produced by immune cells in combating a viral infection.
These are only speculations at this point, but they are the possibilities I can think of for meshing XMRV with the GD-MCB hypothesis. I look forward to seeing the results of more research on this retrovirus.
Oh, I am interested. I am having my autistic children tested for that. I am taking them in the next 1/2 hour to have their blood drawn but might delay to also get them tested for XMRV. I am worried that if they draw the blood tonight (Friday night), the lab will not receive it until Monday and I am not sure if the XMRV test will be effective. They are also getting other tests done as well. Did any of you (that tested for XMRV) get their blood drawn on a Friday? Does it matter?I'm XMRV+ and don't have mercury issues (been tested over decades using various methods)
I do have a mutation in MTHFR though
Just tossing it in for anyone interested
Oh, I am interested. I am having my autistic children tested for that. I am taking them in the next 1/2 hour to have their blood drawn but might delay to also get them tested for XMRV. I am worried that if they draw the blood tonight (Friday night), the lab will not receive it until Monday and I am not sure if the XMRV test will be effective. They are also getting other tests done as well. Did any of you (that tested for XMRV) get their blood drawn on a Friday? Does it matter?
It's most likely the other way around. I would think that a Methylation Block would allow viruses to take over.
Hi Rich and Gerwyn, have a look at this:
"...MicroRNAs (miRNAs) regulate gene expression by base pairing with target RNAs, leading to their cleavage in plants or translational inhibition in animals. Now evidence has emerged that in moss, miRNAs can also silence gene expression at the transcriptional level by interacting with DNA, leading to methylation. This discovery broadens the regulatory influence of miRNAs, and the mechanism may also be applicable to other organisms... ... As ABA is a mediator of stress signalling, these results suggest that miRNAs might epigenetically regulate stress-responsive genes.
The physiological regulation of this epigenetic miRNA-induced silencing pathway and the conservation of miRNA pathway components among species suggest that this mechanism might be generally applicable — a topic for future investigation." http://www.signaling-gateway.org/update/updates/201003/nrg2755.html
XMRV DOES integrate near host miRNA sites....
also some viruses encode their own miRNA - this is now thought to be one of the key mechanisms for herpesvirus takeover of the cell machinery. Not sure if XMRV encodes any of those, anyone?
MicroRNAs and their role in viral infection http://www.springerlink.com/content/367k5n024g0x26r6/
natasa do you know exactly where the integration site is is it in the start codon or anywhere upstream of that?