Hi Koan,


Quote Originally Posted by Koan View Post
Thank you MUCH Lansbergen -- that was a grefat read!

It just freaks me out how much sense it all makes after nothing making sense for such a long, long time.


+1 and here is a quote that may generate some interest, about half way:



Answer by Dr. Judy Mikovits:

I am extremely optimistic that treatment of XMRV or its immune target(s) will restore CFS patients to at least 85% of the original health status even in the sickest of the sick. I base this optimism solely on the level of health that was achieved in HIV AIDS patients with the advent of highly active antiretroviral therapy (HAART) (..)

Plus quite a few good questions and other interesting answers: Real science.



(My bolds, all)

Another one:



Q: In families with more than one CFS (or other chronic illness), is there any indication that XMRV was transmitted to immediate family members?

Prof. Garth Nicolson
The Institute for Molecular Medicine

A: YES…lots of them and I have not looked at everyone but my knowledge of the 101 in the Science paper is that more than 2/3 of them have family member who are infected and MOST are ill perhaps with another overlapping chronic illness..for instance FM and CFS or CFS mom and autistic kids and the cancer in some of the families is frightening

And one more, for some relief for some:



Q: How do you see HHV-6 and XMRV interacting?

A: There are no data to suggest that HHV6 and XMRV directly interact in any way. XMRV is a simple retrovirus so it encodes only structural proteins and not transacting factors like HIV and HTLV.

And yet one:



While our knowledge of HIV disease is useful in developing hypotheses and studying potential mechanisms of HIV pathogenesis, XMRV is totally unlike HIV and HTLV-1 in that it is a simple retrovirus the first ever identified human exogenous simple retrovirus and the family of viruses most closely related to XMRV causes neurological diseases and cancer very by mechanisms distinct in many aspects from HIV and HTLV. We discussed earlier XMRV may be much more stable in body fluids other than blood and cell free and would completely explain clusters and sporadic transmission as seen in CFS both in the US and UK

And yet one more (yea, real science IS fun):



The most important thing to do is identify everyone infected and stop the spread and replication of the virus in every individual prevent disease in those who are well and stop the progression and restore the immune system in those who are ill.

Was somebody suggesting this is good stuff? Or that we need medical/psychotherpeutical 'exercise'-programs?!



Q: Given the association of XMRV with patients whose blood was stored at WPI, how many other docs have sent samples that are positive?

A: Contrary to the assumptions and misinformation about the samples in the WPI repository. These samples were NOT solely from the incline village outbreak. All samples were drawn from patients coming to Sierra Internal medicine between 2006 AND 2008. Fewer that 20 of the 101 were from the original outbreak and more than 75 were sporadic cases of CFS from patients who came to Dr. Peterson from 12 states and Canada. The 101 were representative of patients satisfying CCC and Fukuda criteria throughout the US. At least 5 doctors from across the US including Dr Klimas and Dr Cheney had patients in the repository and in the study. The 101 patients were selected at random from the hundreds in the repository. The main consideration was that we had samples that could be cultured (retroviruses cannot multiply unless a cell divides and several samples from a given patient.

Q: Are your “hit rates” different in the samples sent to you since the Science paper?

A: Not as long as the physicians sending the samples are diagnosing as Dr Peterson does on CCC criteria. In fact the hit rates from overlapping diseases more than we expected now ~35%.

This is getting to be a habit...



Q: If XMRV is actively being transcribed, is there a difference in lab parameters and symptoms compared to those who carry XMRV but are without transcription?

A: We don’t have these data yet but that is a testable hypothesis.

Q: If XMRV is present but inactive, are there any suggestions as to what could be a trigger for (re)-activation?

A: Estrogens, Androgens, Cortisol (stress) and inflammation.

Q: Given the problems with antigen presentation seen routinely in so many patients with chronic fatiguing illnesses, we would expect to see some patients with culture (+) XMRV who are antibody negative?

A: Yes! We see lots of those…these data are very interesting and suggest immune therapy including antibody therapy may be most useful in this disease.


Q: I heard that there may be another study in the U.K. that came to a different conclusion about a possible link between CFS and XMRV. Can you comment on the differing results, and whether the results of the two studies can be reconciled? Thank you.

A: The negative studies were technically flawed in that their methods were demonstrated NOT to be capable of detecting XMRV. Their patient populations likely did not satisfy CCC criteria and they looked only by PCR on genomic DNA the least sensitive way of detecting XMRV. To date none one has attempted to replicate our study. It is very clear that the prevalence of XMRV in UK is NOT ZERO and that XMRV has been detected in CFS patients in the UK.

Take that, MClure & Wessely! O, I ♥ love ♥ real science!