Hi All,
I was at the symposium, but arrived a bit late and missed more than half of F.Ruscetti's presentation. However, I must admit, there was more news after the symposium. I was a bit lucky, meeting a professor who I knew from a University clinic and he started to talk with Prof. De Meirleir
.
What has been told during the symposium ? Let me say that Prof. De Meirleir didn't give a presentation, officially because it was too cold in the auditorium, unofficially, because they want to stay 'low profile' for the time being and let other scientists do their (positive) work.
1) F. Ruscetti talked mainly about prostate cancer and how they detected XMRV in the urine. They tested the urine for mitochondrial mouse DNA, and there was no, so contamination was no issue. They found antibodies against enzymes P12 and P30.
He also questioned why there have been 'negative' studies:
- it could be due to geograpical reasons
- sequences not recognised
...
But, he clearly states, antibodies have been found and they were also able to detect 'viral' proteins. He concludes with the following (retoric) question: where are we now ?
If no ancestral XMRV, then XMRV originated from:
- lab spreading
- from cancer research
2) J.Mikovits
She mainly repeats the original paper from Silverman and her research, about the 67% and 4% findings in CFS and healthy controls. She also refers to the Lo + Alter papers, who detected other MLV gene sequences. The research she did on a UK cohort, clear gag sequences where identified of PLMV's. More than one strain in one individual was detected.
Next, she talked about a clear blueprint of the XRMV, the cytokines profile. This has been already mentioned here on the forum, I didn't had the chance to write it down. Here are some figures:
- IL-8 ++
- MIP-1B++
- TNF-alfa +
- MCP-1 +
- IFN - alfa - (Stimulates machrophages + NK-cells)
...
According to her, it clearly demonstrates a neurological disease.
On Lymphocyte populations she mentioned the following:
CD3- CD56+, NK-cells are reduced and CD3+ CD56+, NKT-cells are increased. As in HIV, where the CD4/CD8 ratio tells you something about your immune function, she has found a similar ratio within CFS: NKT/NK ratio. This ratio could be used to monitor eventually therapy.
J. Mikovits did some research on ARV's and this ratio: after 3 months on ARV, NK-cells clearly increased, while NKT- cells decreased.
B-cells populations:
CD19+, CD20+, CD23+ percentages cells are higher in XMRV+, and most importantly, she thinks that CD20+ cells might be one reservoir!
APOBEC3G
This cell antiviral-system attacks viral RNA, makes the virus hypermutate, but it doesn't render the virus not infectious. It still remains infectious.
Conclusion: XMRV is NOT dead.
Some questions from the audience:
- Did science reply on the mail of J.Mikovits(to retract the XMRV-paper) ? No,. they didn't.
- What will convince J.Mikovits to accept XMRV is dead ? When it's not possible to replicate her work, then it's over. But she's very confident, she said.
3) Maureen Hanson
First, her research is not finished yet, it will somewhere in the summer, however. She demonstrated clearly that her lab did everything to avoid contamination. For me, this was one of the best presentations.
To rule out contamination, they mixed mouse DNA with human and it clearly gives different GAG-sequences as shown by the contamination papers.
She researched a New York cohort and clearly found DNA more similar to PLMV's than to XMRV. She said that primers based on XMRV, might not detect other strains...
On serological testings, more precisely antigene testing, she differentiated 'severe CFS' and 'recovered CFS' from controls.
Conclusions: They clearly detected PLMV GAG-sequences. The future will tell us wether MLV's exist in prostate cancer and CFS.
4) Cecilia Cabrera from Irsi Caixa Foundation, Barcelona
Also a very interesting presentation, from a well experienced researcher. She mainly talked about XMRV in the Lymphoid tissue.
They carried out several tests in vitro, with lymphoud tissue to demonstrate whether XMRV is restricted in the lymphoid tissue or not. The clear answer was no, it clearly divides in cell tissue. However, they demonstrated that the virus was blocked in Lymphoid tissue by ARV's, AZT and Raltegravir.
Also, they showed that after 16 days, XMRV was already in the lymphoid tissue, and by that time, IL-8 started to raise, and this suggests a pathogenic effect, what made J. Mikovits reply that they know very little what happens in the acute phase of the infection.
Finally, K. De Meirleir closes the symposium because it got late already and it was cold in the auditorium.
During the symposium, I spotted a Professor who I was in contact with, and I was really surprised by his presence. One year ago, I had a chat with him and his view on CFS was that it was NOT infectious, and generally (psycho)somatic.
So, I talked to him, and suddenly Prof. De Meirleir joined our conversation, passing us informal information:
- J. Mikovits will not publish for a while, neither will he. They want to stay low profile. It's all about tactics. He knew, the next 12 months, 10 POSITIVE papers will be published, 3 from Germany...
- Prof. De Meirleir fully sequenced an XMRV and another strain from stomach biopsies. However he said, the first samples were not good to detect XMRV, they needed the layer deeper in order to detect XRMV. Because it replicates there happily.
- Prof. De Meirleir agreed with the other Professor, that fully sequenced viruses needed to be in the official gendb. Until now, J. Mikovits keeps it in her gendb, which creates more doubt about her findings.
- Prof. De Meirleir also agreed that science has to do it's work, but that it's unlikely that XMRV doesn't mutate like other retroviruses do.
I've audio recorded most parts also on my iphone, maybe I'll try to add that too, if someone is interested.
OS.
