I came across this abstract recently and found it very intriguing, especially in the context of some of your comments on this blog:

VIRAL SEQUENCE INTEGRATION INTO INTRONS OF CHEMOKINE RECEPTOR GENES

Viral DNA sequences are able to integrate into the non-coding DNA sections of the genome of human cells which have been infected, either spontaneously or experimentally. We have made a data-base search for integration events of non-endogenous viruses into the introns of chemokine receptor sequences. A BLAST search of all viral DNA sequences, using the intronic sequences as “Query,” returned several significant alignments. However, due to the high reiteration rate of the non-coding sequences in the human genome, it became necessary to re-examine the individual alignments to verify whether the virus-flanking intronic sequence was really located in a chemokine receptor intron. We found only one unquestionable event of viral insertion of a section of a long terminal repeat of the murine leukemia virus within the first intron of the CC chemokine receptor 7 gene. Possible biological effects of such an insertion are discussed. Further experimental or clinical research could demonstrate the occurrence of other intronic viral insertions in human chemokine receptor genes. Maria Antonietta Panaro, Immunopharmacology and Immunotoxicology, December 2009, Vol. 31, No. 4, Pages 589-594

If XMRV does something similar, i.e. integrates within/nearby chemokine receptor sequences … and thus affects their expression levels, wouldn’t that help explain quite a lot of XMRV pathogenicity in CFS (and indeed autism, which is my primary area of interest), even in the absence of any replication activity? Raised levels of certain chemokine receptors would make one more susceptible to infections by other viruses that are implicated in CFS and autism (and whose raised levels are also implicated in susceptibility to neurological damage/autism symptomatology caused by HIV for example).

I’m aware that this is all very speculative at this point but would appreciate your input.

Somewhat off-topic:

My wife is a long time PWC, which also suffers from severe angioedema. Her angioedema is said to be explained
by her positive autologous test. The autologous test (ASST) is the one in which one's serum is injected back
subcutaneously, looking for an allergic reaction.

It's hard to assume her problems are not related. Can you think of any mechanism by which XMRV
can explain the ASST results?

Much obliged
Ronen

I would really like to know the possible consequences of late vs early treatment! I am late in the game….what are the implications of having a larger XMRV reservoir in my body even on antiretrovirals? Does this mean less immune reconstutition? More cancer risk?

Also, how would one measure immune recovery in CFS? CD4/CD8 ratio? RNase L activity?

Thank you!!!!
Sue

Thanks,

Dan

Given what you know of XMRV, is there anything you can suggest for us *now*, as in over the counter supplements that might inhibit XMRV?

Best,
Rrrr

Since XMRV replicates slowly, do you think, if we take AZT or some drug, it will take us a long time to get better? how long do you think it would take? Do you think, from what we know so far, that one drug will be enough?

Love your blog

Once I had my “% specific lysis” tested at VIP Dx. It was abnormal. Does this imply that the virus is replicating?

ME/CFS has kindly posted the Dr. Coffin comment. Why did he say that the slow replication will impact treatment? Is CFS caused by replication of XMRV or the proteins it pumps out during latency?

Thank you

I think the “licensed” part in there refers to anti viral drugs in general and ten of those have been evaluated for activity against XMRV.

“It’s not that this virus has a lower mutation rate than HIV. These viruses probably have all about the same mutation rate. But its suggestive in fact that there are very few cycles of replication that separate the viruses that’s in one person from the virus that’s in another.”

” And in some ways the implications of that are both good and bad news. The bad news is that it suggests the virus is not actively undergoing ongoing replication during the course of infection of a single individual and that would not be good news if one were trying to use antiviral therapy. “

I ask because Dr. Coffin mentioned that slow replication(?) of XMRVwould make treatment problematic because present drugs target replication, as in HIV… So I guess I wanted to know how the differences between XMRV and would impact treatment.

also, if the virus is just sitting there pumping out proteins(?) could the antiretrovirals still do something?
thank you for your time

I understand that XMRV replicates so slowly that treating it will be diffcult. Does this mean that Isentress or AZT will not work at all or will it just take much longer for a patient to feel better on the drugs?

Virology. 2009 Dec 1. [Epub ahead of print]

means it will soon be available in full.

Thanks for your on-line course. I intend to work myself through it as a CFS patient of 39 years, it is important that I understand everything I can about viruses. If XMRV is indeed key, I need to understand as much as I can to work out a treatment protocol.

You are right, of course, scientific illiteracy is dangerous in the extreme.

Pamela B.