I think something has been missed in Dr. Mikovits Talk. I think she actually presents a pretty compelling bit of evidence that however XMRV came about it that it really has infected the patients who's samples the WPI has tested.
XMRV has alot of issues right now - but her idea seems solid to me. Check out the signature section.
"Finding A Signature of Infection - Then she presents a simple but seemingly compelling answer to the contamination question. Researchers know that the APOBEC enzymes in human B and T-cells switch out amino acids in XMRV rendering it unable to replicate (in T-cells). Right now a good chunk of researchers appear to believe that XMRV is a laboratory creation that got into human samples but not humans. Geneticists are arguing that low variability in XMRV indicates it is not in humansbut what about a more direct measure? What about showing that the XMRV in your sample bears evidence of being altered by human enzymes..ie the APOBEC enzymes?
Finding sequences that are consonant with APOBEC editing is like picking up a signature indicating that XMRV has been in a human body. In the next slide she shows evidence of just that; hypermutation of XMRV sequences found in B-cells taken from human samples.! Dr. Mikovits focused on APOBEC editing almost a year ago noting that Grooms finding that such was going on enabled them to adjust their testing to better pick up XMRV. There are so many factors in XMRV that its hard to know how any one will play out but on the face of it makes sense that any XMRV that shows evidence of APOBEC editing should have infected humans at one time. It appears to be a strong argument that XMRV she has found has infected humans.
Then she shows that B-cell lines in humans can carry versions of XMRV that have been altered but can still replicate. Thats a big deal because other than the prostate nobodies been able to show a place where XMRV replicates. Its also intriguing given the fact that EBV replicates in these cells as well and with the interesting study on Rituxumab (B-cell inhibitor) going on in Norway."
In this context, could someone with a little more scientific background that me consider how this ties in with this Steiler and Fischer paper?