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Er dette forklaringen på hvordan XMRV forårsaker ME?

Artikkelen som ScienceNOW publiserte 6 januar førte til et langt og interessant kommentarfelt. En av kommentarene utmerket seg med en god potensiell forklaring på hvordan XMRV forårsaker ME. Hvor nært dette blir den forskningsbaserte forklaringen gjenstår å se:

«WPI’s finding of XMRV in CFS offers the possibility of blowing away a lot of smoke. I expect it to ultimately stand up. XMRV attaches to a protein called XPR1, a G coupled protein receptor also known as GPR1. In general, its ligand isn’t known. It has homologues in all known animal and fungus genomes. It’s found in both cell membranes and mitochondrial membranes. It’s found in the cell membranes of yeast, although, as far as I know, yeast cells don’t communicate with each other. When the gene is messed up, mitochondria are malformed.

In the nematode C. elegans GPR1 plays a role in the development of synapses. It appears on the presynaptic cell. When activated by the post-synaptic cell, it sets in motion the development of presynaptic vesicles. As it does this, it removes itself from the cell membrane in the vicinity of the synapse.

In human cell cultures, XPR1 rna is most strongly expressed in mitochondria-rich cells that normally have growth and turnover. It apparently doesn’t appear strongly in mature CNS cells however. It’s strongly expressed in blood vessels, all muscles, young brains, and kidney cells.

XMRV is known to infect leucocytes. I haven’t seen that it prefers natural killer cells, but I expect that to turn out to be the case.

Viruses closely related to XMRV are known to cause degeneration of neurons.

XMRV reproduces more slowly than HIV.

Now for the reckless speculation: XPR1 was originally for controlling mitochondria, and it only appeared in cell membranes when it got lost. Later, the cell hijacked it for the formation of synapses. In order for that to work, it had to withdraw it from the cell membrane when its work was done.

So here you have:
1. XMRV attacks leucocytes and especially NK cells, impairing the ability to fight normally dormant viruses and some other pathogens.
2. It attacks some nerve cells that have relatively high turnover, resulting in orthostatic hypotension, blood-vessel related heat and cold intolerance, weakness in smooth muscles, irritable bowels, and sometimes pain.
3. In children, it attacks some neurons in the developing brain, resulting in autism.
4. Inside cells, XMRV surface proteins attach to receptors on mitochondria, disrupting their functions.
5. Because some of the cells that are supposed to be killing XMRV are attacked by it, there is a potential for a controlled XMRV infection being flipped into an uncontrolled one by stress, poor diet, watching the late late show, other diseases, etc.»

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