Dr. Peterson's Testimony at the CFSAC in Text

dannybex

Senior Member
Messages
3,369
Likes
2,369
Location
Seattle
Thanks Cort...

This was news to me...

"With XMRV it was important to differentiate it from all the other mouse retroviruses that are in the family of the gamma retroviruses. And this phylogenetic tree that was developed by gene-sequencing, demonstrated that this particular XMRV that we isolated from the Chronic fatigue patients was similar to, but not identical to, the XMRV that has been demonstrated in patients with prostate cancer..."

For some reason I thought it was the same thing.

And this was also surprising:

"We did look at the genetic variation in RNASE-L that had been reported in the prostate cancer patients. Its a fairly common genetic abnormality in the population at large. And in fact we did not see any correlation with the patients who were positive. "

Finally, the following seems to contradict what he told you after the conference:

"And so you can generate a hypothesis much like the HIV hypothesis is that you get an acute infection, you develop an antibody response, ultimately you have a failure of the immune system and we postulate here that maybe in NK-cell numbers and function resulting in very significant and prolonged disease."

Is my brain completely rotting, or didn't you say Cort that he believed a weakened immune system comes before XMRV infection?

thanks,

d-bex
 

Cort

Phoenix Rising Founder
Messages
7,361
Likes
2,065
Location
Arizona in winter & W. North America otherwise
This

"With XMRV it was important to differentiate it from all the other mouse retroviruses that are in the family of the gamma retroviruses. And this phylogenetic tree that was developed by gene-sequencing, demonstrated that this particular XMRV that we isolated from the Chronic fatigue patients was similar to, but not identical to, the XMRV that has been demonstrated in patients with prostate cancer..."
Surprised me as well. Its really hard to figure out what's going on. Is it so similar to the XMRV in prostate cancer that they are essentially the same or is it different in significant ways?

"We did look at the genetic variation in RNASE-L that had been reported in the prostate cancer patients. It’s a fairly common genetic abnormality in the population at large. And in fact we did not see any correlation with the patients who were positive. "
This brings up another interesting point. Apparently the genetic variation RNase L. that inhibits its activity is fairly common but what about the RNase L dysfunction found in many chronic fatigue syndrome patients? We have two different abnormalities here - both appear to inhibit RNase L functioning but probably n different ways and in different degrees. Now I'm not clear whether both RNase L. problem are not a factor in XMRV; perhaps the RNase L dysfunction in chronic fatigue syndrome does contribute to it.

Yes, I was a bit surprised by that statement as well. I guess its all conjecture at this point whether the virus comes first or the immune dysfunction. He told me that his guess was that an immune weakness (plus other problems?) comes first but here suggested that the other could be true. Hopefully someday we'll know!
 

Esther12

Senior Member
Messages
13,774
Likes
28,351
Arround the time of the initial announcement I remember virologists mentioning the differences with prostate-xmrv, and saying that the differences were very small, and indicative that the virus had probably moved to humans relatively recently (within the last century or so).

All with the usual provisos about this being very preliminary guess-work.
 

garcia

Aristocrat Extraordinaire
Messages
975
Likes
247
Location
UK
This surprised me as well. Its really hard to figure out what's going on. Is it so similar to the XMRV in prostate cancer that they are essentially the same or is it different in significant ways?
The value of having the transcripts is that we can answer questions like this. From Dr Coffin's testimony (yet to be posted):
"One of the most very striking things is the very close relationship, and Dr Peterson showed you this and I’ve also got that on the slide in a minute, of how close these viruses are to one another. And the most distant pair actually, both of which were from prostate cancer, differs by only 0.3%."
In other words all these various strains isolated so far from prostate cancer & CFS are the same virus, XMRV, but with minor variations (as you would expect in a mutating virus). And actually as Dr Coffin says the most distant pair are both from prostate cancer. So its not like there is one strain in prostate cancer, and one strain in CFS. There are lots of strains across both diseases, but you can't necessarily separate the strains by disease. If you could easily seperate the strains by disease then the most distant pair would be one from CFS and one from Prostate Cancer.

Dr Coffin goes on to say:

"Now a patient who's been infected with HIV for one or two weeks has a greater diversity in his virus population than does virus isolated in different years, different parts of the country, different diseases of this virus. It’s really remarkable how close that is and that’s a very important implication. 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."
 

starryeyes

Senior Member
Messages
1,555
Likes
69
Location
Bay Area, California
Thanks for the explanations about the differences found in XMRV in Prostate Cancer vs CFS, garcia and Esther. I have been wondering about this and got answers here many weeks ago but forgot the particulars that were in the replies.

garcia it's great to have Dr. Peterson's testimony in written format. I keep falling asleep when I'm listening to the video. Not because he's boring, btw, I'm riveted. It's just another one of my symptoms.

tee
 

rebecca1995

Apple, anyone?
Messages
378
Likes
232
Location
Northeastern US
320 v. 218 controls

Dr. Peterson talked about 320 controls at CFSAC, but the Science paper uses the figure 218.

Any ideas about the cause of this discrepancy?

Dr. P., from transcript:
There were 320 control samples that were roughly matched by age and sex and geographic distribution. I point out that these control specimens were not contact-controls, laboratory workers, family members, etc, which would strongly probably bias the findings on controls (potentially).
 

Dolphin

Senior Member
Messages
17,555
Likes
28,235
Dr. Peterson talked about 320 controls at CFSAC, but the Science paper uses the figure 218.

There were 320 control samples that were roughly matched by age and sex and geographic distribution. I point out that these control specimens were not contact-controls, laboratory workers, family members, etc, which would strongly probably bias the findings on controls (potentially).
Any ideas about the cause of this discrepancy?

Dr. P., from transcript:
218 controls plus 101 patients is 319 in total. My guess is that is what Dr Peterson was referring to (he might have round 319 to 320 in his head or there might have been a problem with one of the samples).