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Is it possible that disease stage makes a difference in detection of XMRV and have any XMRV studies tested patients for the virus at several different points over a period of time?
How different or similar are your methods from the Science paper or the amended version of the WPI's methods: http://www.iacfsme.org/BULLETINSPRING2010/Spring2010MikovitsLetter/tabid/427/Default.aspx
Since the Science paper was published at least six papers have been published that were unable to find it and several other studies have reportedly failed. Have there been other retrovirus (or virus) studies which the scientific community initially experienced a similar degree of difficulty validating but later did validate?
What new information will your study bring to the table? When do you expect it to be published?
Are your results validated against a positive human sample?
Did you receive XMRV samples from the WPI and if so were you able to validate the presence of XMRV in them?
Our understanding is that you gathered samples from patients rather than used stored samples. Is this important and why?
1. Do you think that XMRV is the result of vaccines (either human or pet) contaminated with animal retrovirus?
2. Do you think that XMRV could have "dropped into" or "piggybacked onto" a herpes virus like HHV-6 or EBV, which allowed it to be spread casually?
3. How can cluster outbreaks of CFS be explained?
4. Could an escaped engineered virus be the cause of XMRV?
5. Can you please explain how XMRV affects the female urogenital system?
In your studies of XMRV, what kind of tests have you found to be most successful at finding XMRV in blood? Do you think culturing the virus makes a difference?
XMRV growth is stimulated by androgen. If XMRV should be shown to be the cause or a co-factor in chronic fatigue syndrome, why are most (like 4 to 1) CFS patients women? And related to that, the macaque monkey studies showed that XMRV has a tropism for prostate tissue; do we know what tissues it prefers in women?
Could XMRV cause immunosuppression, and if so, how?
In the studies on macaque monkeys, XMRV viremia in the blood cells peaked at about day 8 after infection, and after a couple of weeks it was almost gone from the blood. Since finding XMRV in the blood seems to be difficult, is there somewhere else we should test for it? Like maybe saliva or respiratory secretions?
My question for the brilliant Dr Singh is,
If xmrv is it! then when would drugs be available to treat us, if everything went to plan! (months, Years or decades?)
I was very encouraged to hear that you are engaged in a major study of the XMRV in Chronic Fatigue Syndrome with Dr Bateman and Dr Light.
1. Could you give any indication please of just how close you and your colleagues might be to proving that the XMRV causes CFS, or whether we are still at the stage of proving strong association only?
2. If strong association only, what kind of studies do you think we might need to discover whether there is causation?
3. Where in your view is the most likely reservoir for XMRV in CFS patients, other than in the peripheral blood?
4. Is the reservoir likely to be the most practical location from which to harvest XMRV samples and develop tests for use in a clinical setting (ie clearly saliva or blood tests are more practical, but what if the main reservoir is the brain or the nervous system?)
Thank you both very much!
The UK may seem a world away to you all at this present time, but I can assure you that CFS labelled patients over here are enthusiastically following all promising scientific developments in this field worldwide and are very grateful to you and your colleagues for undertaking this groundbreaking research and for your scientific curiosity.
In treating XMRV, some of us are considering getting stem cell treatments. Do you think HAART would hurt the new stem cells we get?
What can you tell us about the XMRV assay being used for the Stanford/Columbia study?. How is it similar or different from others?
Thanks so much, and for all of your work on XMRV/CFS, especially!
I was wondering if Dr. Singh could comment on your show if XMRV may be present in cancers other than prostate cancer. I am interested to know specifically if it may be a factor in the development of cervical cancer in women. Is there any chance XMRV could act as a trigger and interact with a person's genes and HPV (and factors like smoking) to create cervical tumours? Also, if there is time could Dr. Singh comment if XMRV triggers the expression of Herv's (endogenous retroviruses) in cancer and other disease?
Thank you for covering this important topic on Twiv. I am a new fan.
- Can you provide us with a rough indication about when we can expect the publication of your XMRV/CFS study?
- In case XMRV causes CFS, to what degree do you expect people with CFS to recover, given the right treatment (not the treatment available now, but any future one)?
Would it be expected that XMRV would have a similar disease effect as the related viruses in mice (SFFV, MULV).
If that is true, could we expect that the reason we see various outbreaks and susceptibility to XMRV be the same as in mice?
For example in mice (as summarized by http://jvi.asm.org/cgi/content/full/83/21/11211) SFFV vulnerability can be either genetic or affected by a co-infection. If XMRV also turns out to facilited by a co-infection could that cause the observed clusters? For example some other virus (most likely one of the ones people have thought actually caused the disease over the last 20 years) infects a bunch of people in an area and as a result a group there who are already carrying XMRV now get CFS?
Also given that there seems to be a high rate of thyroid problems and perhaps thyroid cancer in people with CFS could this also be a result of the virus. For example if certain people have a genetic variance of MET it could be activated by XMRV and cause cancer to kick off?