German study finds xmrv

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XMRV doesn't exist in the UK according to Wessely & McClure - they say. ''If it was there, we would have found it''. And the other classic: "We are confident that our results show there is no link between XMRV and chronic fatigue syndrome, at least in the UK. Egg on face much for the Imperial College London I think. I wonder how stupid they will look in the next few months!!!! Did they really think no one else would bother looking at XMRV?

Don't have a go at him. Hes aways looked stupid . Heres a link with picture called How people can think themselves sick

http://www.google.co.uk/imgres?imgu...mage_result&resnum=3&ct=image&ved=0CBwQ9QEwAg
 

serenity

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Hi Esther12,

It seems to me that the linking of CFS with XMRV will become less important as more research is done. I don't think we need to even know that XMRV causes CFS. It just has to be shown that XMRV can cause illness. Then if you are diagnosed with XMRV (which 98% or more of us might be) than we can start ant-retroviral treatment. So based on these assumptions my plan is:

1. Get tested for XMRV as soon as there is a reliable test.

2. Wait until it has been determined that XMRV causes illness (which should be relatively simple given all of the people with CFS out there).

3. Contact a Doctor who specializes in Aids patients to get the latest anti-retroviral combinations. It will be good to go to a Doctor who doesn't care whether I ever had CFS!

It sounds kind of simplistic and of course research will have to be done to find the best treatment but this is what I am hoping for.

Lynn
i'm with you Lynn, this is exactly my plan as well :)
 

Esther12

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Hi Esther12,

It seems to me that the linking of CFS with XMRV will become less important as more research is done. I don't think we need to even know that XMRV causes CFS. It just has to be shown that XMRV can cause illness. Then if you are diagnosed with XMRV (which 98% or more of us might be) than we can start ant-retroviral treatment. So based on these assumptions my plan is:

1. Get tested for XMRV as soon as there is a reliable test.

2. Wait until it has been determined that XMRV causes illness (which should be relatively simple given all of the people with CFS out there).

3. Contact a Doctor who specializes in Aids patients to get the latest anti-retroviral combinations. It will be good to go to a Doctor who doesn't care whether I ever had CFS!

It sounds kind of simplistic and of course research will have to be done to find the best treatment but this is what I am hoping for.

Lynn
Hi Lynn

That could take quite a while though. Getting a standardised and accurate test in probably the tricky part - from there, linking XMRV and CFS would be easy (presuming that there is a link). This trouble with XMRV detection has been going on for quite a while with prostate cancer... who knows when it will be worked out.

Hopefully we'll have more news on XMRVand CFS coming out as they're still developing and perfecting testing techniques. I think it will be quite a while before insurance plans or state health services are going to be paying for XMRV tests.
 

anciendaze

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looking at this from a different angle, not just CFS

After studies which showed 0% incidence in the UK led to an editorial in BMJ only a few months ago somberly burying XMRV, and after a German researcher was quoted as saying "there is no XMRV in Germany", this is a serious embarrassment. This is also where the vague nature of the Oxford definition will become a two-edged sword hurting those who use it.

If they can't exclude everyone with XMRV from a cohort based on a psychiatric definition of CFS/ME, (as we know from samples also tested by WPI,) they almost certainly can't exclude XMRV from a cohort of clinically depressed patients. This will mean reevaluation of accuracy of diagnosis and effectiveness of many kinds of therapy for real psychiatric problems, their core area of expertise.
 
R

Robin

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After studies which showed 0% incidence in the UK led to an editorial in BMJ only a few months ago somberly burying XMRV, and after a German researcher was quoted as saying "there is no XMRV in Germany", this is a serious embarrassment. This is also where the vague nature of the Oxford definition will become a two-edged sword hurting those who use it.

If they can't exclude everyone with XMRV from a cohort based on a psychiatric definition of CFS/ME, (as we know from samples also tested by WPI,) they almost certainly can't exclude XMRV from a cohort of clinically depressed patients. This will mean reevaluation of accuracy of diagnosis and effectiveness of many kinds of therapy for real psychiatric problems, their core area of expertise.
I was thinking that too, they should have found something. I went back and took a look at the Groom study which found XMRV "neutralizing activity" in the serum of some of the control patients and 1 CFs patient.

This is what they said:

In our serological studies we have also identified
neutralising activity against XMRV in around 4% of
all the samples examined. Remarkably many (but not
all) of the seropositive samples were identified in a relatively
small group of blood donors within the SGUL
cohort, possibly suggesting a local outbreak of infection.
There is no evidence that this group are related or that
they have a particularly high risk of acquiring a retroviral
infection. Therefore, an outbreak of this kind
seems unlikely.
The one serum that failed to neutralise
VSV-G pseudotyped MLV was, however, able to
neutralise MLV particles pseudotyped with other retroviral
envelopes. We therefore consider these positives
from healthy blood donors to be non-specific cross
reacting responses.

Although we cannot rule out the
possibility that the activity of these samples against
XMRV is also non-specific, one possible explanation for
these serological findings remains that XMRV infection
has occurred in around one percent of the population.

This figure is consistent with the general prevalence in
control samples previously reported.Given the common
oncogenic properties of gammaretroviruses [19] and the
reported link between XMRV and prostate cancer [1,5],
such an observation might be of considerable significance,
particularly for the blood transfusion services
.
So they did find it, just not significantly in CFS. They weren't even sure that it was XMRV at all -- what they found might have been specific to something else because ALL of their samples were negative for PCR.

It's interesting that the German study didn't involve blood!
 

Otis

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Hi Lynn

That could take quite a while though. Getting a standardised and accurate test in probably the tricky part - from there, linking XMRV and CFS would be easy (presuming that there is a link). This trouble with XMRV detection has been going on for quite a while with prostate cancer... who knows when it will be worked out.

Hopefully we'll have more news on XMRVand CFS coming out as they're still developing and perfecting testing techniques. I think it will be quite a while before insurance plans or state health services are going to be paying for XMRV tests.
Isn't it feasible/logical that XMRV researchers might seek out ME/CFS patients for study IF we get at least one more solid study showing a high degree of correlation between ME/CFS (CCC cohort) and XMRV?

To study the virus one must go where it lives and we may be the best place to look, even if they don't care about ME/CFS per sea.

I don't care why they study us as long as they do....
 

anciendaze

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don't forget Judy's results

...
So they did find it, just not significantly in CFS. They weren't even sure that it was XMRV at all -- what they found might have been specific to something else because ALL of their samples were negative for PCR...
Dr. Mikovits tested samples from both the Groom study and from the Nijmegen group study, and did find XMRV. Because the controls in that third study often came from the same family, so that infection without symptoms was fairly likely, the "false positive" she got might also be real. Add in "CFS" cases which could have been depression without infection, and it is possible she correctly identified all seven samples. I don't have numbers for the positives she found in the Groom study.

My conclusion after looking at all three papers was that the first could have missed the virus by about two orders of magnitude in sensitivity, and the other two were off by about an order of magnitude. Close, but no cigar.

Considering the obstacles introduced by the way they defined the cohort, and the way the samples were stored and prepared, this is remarkable. It now looks like they have publicly demonstrated they could not be sure of XMRV even when it was present.

There was a statement from the Nijmegen group that they were able to find XMRV in a sample provided by WPI, but I didn't see this in the published paper. As far as I can tell, all their positive controls were created by spiking a sample with virus from culture, then diluting it. If they were off on the number of virus particles in these artificial controls, everything fits together in my mind.

The Groom study had very nice real-time quantitative PCR, and seemed to be implying their standards were higher than WPI's. They ended up demonstrating that they had a larger budget, not that they knew how to use it.
 

Lynn

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Isn't it feasible/logical that XMRV researchers might seek out ME/CFS patients for study IF we get at least one more solid study showing a high degree of correlation between ME/CFS (CCC cohort) and XMRV?

To study the virus one must go where it lives and we may be the best place to look, even if they don't care about ME/CFS per sea.
Yes Otis. That is what I am saying. I just listened to the Nevada Newbreakers interview. They said 99% of the CFS patients tested positive for XMRV. Why not see what has caused ilness in this cohort? It makes sense if you are trying to determine what XMRV can do in humans.


:ynn
 
D

dmarie4301

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Off the top of my head, if XMRV can be found in saliva and sputum, then maybe it's not really very significant of a find at all, since anyone therefore should have it. XMRV could be a dead end road, when all is said and done.
 
K

Knackered

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Off the top of my head, if XMRV can be found in saliva and sputum, then maybe it's not really very significant of a find at all, since anyone therefore should have it. XMRV could be a dead end road, when all is said and done.

The point is everyone doesn't have it, ~3% in control samples and 99% in CCD CFS samples. That's what's significant.
 

jewel

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Wow! Nothing really to add here; I just skim read the rest of this thread... had seen it earlier this afternoon. Now I feel brain-dead or at least brain-boggled, but impressed with all of the analysis. So glad that they found XMRV, not in blood but in respiratory secretions, in similar percents as controls of other studies, higher percents in immunosuppressed patients...none to the degree found by WPI in CFS patients. Spark notes for the brain boggled. Did I get that right? Now if another study again finds high percents of xmrv in (well-defined) CFS patients vs. controls, that would be a correlation that would further imply causality... if I am making any sense here.
 
D

dmarie4301

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But we are still waiting for a replication study to confirm what WPI did. Without that and without proof of causation, it's just a bunch of conflicting studies and disagreements. I get that the WPI study had impressive results...but we need another lab to find the same results. Until then, XMRV may be nothing, nothing at all to be concerned about.
 

consuegra

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In regards to Cort's recent XMRV buzz entry, I am reminded of the Viracor Immuknow test which is used for transplant patients. Here is a quotation from my blog on the Immuknow test:
Ablashi’s study of 2005, using Dr. Daniel Peterson’s patient population, tested the functionality of the global T-cell response using an FDA cleared response for cell-mediated immunity assessment (Cylex Immune Function Assay, ImmuKnow) - and these cellular responses were compared to patients with HIV and immunosuppressed transplant patients. The ImmuKnow test was assessed based on the amount of ATP expressed in ng/ml. All three groups has median immune function that was not statistically different. The transplant patients averaged 259 ng/ml ATP, followed by HIV patients at 263 and CFS patients at 281. CFS patients showed consistency with both the transplant and HIV patients - with the majority of patients in the median zone, followed by patients in the low zone, with the smallest percentage in the strong zone. More can be read in Ablashi’s and Krueger’s book Human Herpesvirus-6.

This Immuknow test certainly ties these patients together in terms of this particular immune response.

Chris

http://cfspatientadvocate.blogspot.com
 

Stone

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Is there such a thing as an exogenous human retrovirus that is not pathogenic? If XMRV is found in >95% of people with CFS, what are the odds that it does NOT cause CFS? Anyone?
 

free at last

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the suggestion in the paper is that immunocompromised patients may be susceptible - but that raises the question of what causes the immunosuppresion to begin with, as most of us were healthy at some point

Just saw this, i dont undertand the science very well, but what i did get was immune suppressed people get it more. dont like printing this, but its important so here goes.

I smoked pot for a long time and leading up to the flu like attacks that lead to my diagnosis of ME, ive read that pot can lower the immune response is that correct ? Indeed i had to give up because i felt sure it caused more frequent crashes. (possibly lowering my immune defense )

but still had crashes when i gave up, but not as frequent

what about alcohol ? could this also suppres the immune system. and stress what about that ? what other things could cause someone to be more at risk from xmrv ? in a immuno supressive Way making crashes more frequent, dont know if im positive yet, but am part of the ashford 50, so will find out when published.

this seems exciting news, its in Europe and immune suppresed people have it more, what if immune suppression allows xmrv to do more damage, or indeed cause more frequent crashes, my god this might actually fit, the primates infected with xmrv showed no symptoms. what would happen though with months or years of immune suppresion it might not matter what the suppression is as long as the immune system is compromised. feedback please anyone. Am i way off here. just trying to understand and maybe shed light.
 

Stone

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I'm wondering if the XMRV actually causes the immunosuppression, and that's why it's seen in immunosuppressed people. Like which came first, the chicken or the egg? Maybe the people in the study who were both XMRV positive and had respiratory infection were more prone to respiratory infection because XMRV had compromised their immune systems. Maybe they would not have had the respiratory infection had it not been for XMRV chipping away at their immune system. I had 5 bouts of pneumonia in the year before I got CFS. I also got a tatto shortly before becoming ill. I was also exercising like an insane person, pushing my body well past exhaustion in an attempt to loose weight and feel better, and this exercise was taking place in an outdoor par course that was known for tick infestation and yes, I am positive for Lyme antibodies. I was also experiencing daily exposure to diesel fumes as well, and, yes, was smoking pot a lot too before I got sick. So pick one, pick two, add them all up maybe. I can also tell you that both my sisters have CFS as well as my daughter now and none of them were doing any of those things I just listed, so go figure.
 

starryeyes

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Thanks for sharing free and Stone. I think we also need to remember the large number of children who have severe ME/CFS. Most likely their bodies were not run down by adolescent or adult activities.
 

alex3619

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Hi fellow travellers,

I thought I would post my current interpretation on a big picture, then make some random comments. Much of what I am going to say has been said already on this forum, but it is worth putting together. I am not going to mention who said what as they are so many of you - which is a good thing!

This is my current model of XMRV and ME or CFS. It is only one possible model, and I don't presume it is correct.

The XMRV infected population is perhaps 6%. I have been saying this for months now, but the figure depends on the data used, I get anything from 1.7% up to 9.72%, and my most recent calculation was 5.1%. What is missing from the oft quoted 3.7% is that this is the HEALTHY people. Add in the percentage of sick people (which goes up as the number of diseases it is found in increases, and goes up or down with the latest coprevalence figures). This gives you a true picture.

The suggestion of 10% is not impossible. The Dubbo study showed that around 10% of patients with a severe infection develop CFS. We are also ignoring the very large numbers of patients with post-transplant fatigue and post-cancer fatigue. Fatigue is the NORM in these disorders, and many never recover. Spend some time on the postcancer fatigue forums and you will see that the description is almost identical to CFS, it is just that having had cancer a CFS diagnosis is excluded. These patients have yet to be tested for XMRV (except of course for some prostate cancer patients).

The CFS population is a highly overlapping subset of the XMRV population, but it may not completely overlap. The same is true of the other disorders that are implicated - atypical MS, autism, FMS, GWS etcetera, which may also overlap with each other.

Let me ask a question: if 3 to 6% of the population have XMRV, then what happens during a viral epidemic? Perhaps everyone who has XMRV and a severe infection gets CFS. This is the two hit hypothesis, which I proposed many years ago but nobody was interested at the time (but is popular now that we know about XMRV). It seems to me that first you get XMRV, and then something triggers it - it has androgen and cortisol sensors for a reason! The KIND of trigger determines whether you get CFS or FMS or both, and so on for the other disorders including autism. Genetics probably does play a role, but all of these disorders will have to be examined to look for genetic links with XMRV. From the Incline Village epidemic experience, it has been claimed that it is unlikely that XMRV could cause CFS due to the XMRV incubation period (10 to 21 days). The epidemics simply spread too fast. However, if the two hit hypothesis is adopted, then this problem disappears. The epidemics are just conventional diseases that trigger the underlying XMRV infection and so result in CFS.

(Does anyone know if FMS trigger points correspond to lymph nodes?)

Peterson has commented that he has found that "recovered" CFS patients are not doing well. This is extreme speculation, but it is possible that they suppressed the CFS reaction from XMRV but not the virus - and this has long term consequences. Curing CFS without removing the cause is only a temporary solution.

This would make XMRV cocausal, not a sole cause. It would however also mean that XMRV is a necessary requirement for getting CFS, and result in the kinds of percentages we are seeing, as well as explain both slow (repeated immune insults) and sudden onset CFS (severe immune insult). It would also mean that if you suppress the XMRV completely, you could halt CFS progression, and if you can elimate the viral host cells you can cure CFS (ignoring the problem of genome integration). Of course if something like the Peroxnitrite Hypothesis (Martin Pall's work) is correct, then treating XMRV is only the first step - you still have to shut down the CFS response.

Now, there is the alternative explanation, that we have the same risk of contacting XMRV but are particularly susceptible. I think this is unlikely, as unless we have a VERY specific immune abnormality (eg low NK function, or genetic predisposition) that gives XMRV a serious edge, you should find nearly every transplant patient has the same prevalence of XMRV as they are all susceptible. You should also find a very high prevalence of XMRV in HIV patients. We will see, but this doesn't look likely. It would also not explain the epidemics, unless the specific immune weakness allows for very much shorter incubation periods.


And now for some random comments, all relating to one post or another on this thread:

Lynn (tloyd) is right - if it can be shown that XMRV is pathogenic, we can all be treated even without proof of XMRV causing CFS, as long as we are XMRV positive. The worry is that not all of us will be.

It was noted somewhere on this thread that early studies on prevalence of CFS showed that some professions are more likely to get it. I would like to repeat and expand that list: medical professionals (not just nurses or doctors), teachers, airline pilots, serious endurance cyclists. All of these people have major exposure to viruses, and the cyclists are at risk for overtraining which suppresses the immune system.

I was at a conference in 1999 when de Meirleir discussed the risk of CFS being blood transmissable. For most of the last decade this was ignored. Haemopheliacs are very aware of the risks, just spend some time on their forums. The news that blood products can have XMRV inactivated is very very welcome, and may be a better solution than testing for the virus, although both approaches together would be much better.

I have been worried for months that the combination of XMRV in saliva plus high stability might mean this virus is airborne. I have held back on public forums because I didn't want to cause public panic, and in particular because many with CFS have close family members and the worry could seriously degrade their health - and we don't know for sure yet that it is transmissable this way. In fact, we only know that it can be transmitted by blood contact, everything else is speculation. However, it is looking more and more like XMRV may indeed be airborne, although another possibility occurs to me. XMRV appears to replicate when there is another virus present, or some other immune challenge (injury, poisoning etc). What better place to wait than in the lungs, given how many respiratory infections are floating around?

XMRV has a very very low viral load in the blood, and I suspect the same in the sputum and saliva. It could easily be airborne, but the transmission rate could still be very low. This is because the virus will often die quickly (even if it is stable, the low load will mean there is very little virus present and so is at higher risk of all of it dying). Think of this as a half life - the total number of virus particles halves every so many minutes. XMRV would have a much longer half life than HIV (which has a very short half life, it dies quickly after leaving the blood), but with so few virus particles present it wouldn't take long for all of them to die. The real risk then would be the omniprevalence. With maybe 5% (or pick another number) of the population spreading it all the time, then it will slowly spread to anyone who can't fight it off, then lurk waiting for a trigger. I think Mary Schweitzer said it best, although I may be misquoting her (I don't remember very well): XMRV is to CFS as HIV is to AIDS. Not everyone with HIV gets AIDS immediately, it lurks. There is no reason to suspect that XMRV is any different, and given its low replication rate it probably lurks for much longer than HIV does. If XMRV is airborne, then Humanity is very very lucky it is not very transmissable or we would all have it. Of course if we ignore XMRV then that could still happen, it would just take longer.

I would like to thank Cort for Phoenix Rising and these forums: these have become my first stop after reading my email. Good work.

Bye
Alex Young
 

free at last

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Thank you Starry eyes, I agree that does seem at odds, but does it really mean immune suppression of any kind may not make xmrv stronger, more able to do its dirty work ?

it may not be immune suppression that makes people ill with xmrv like the children you mention, but surely its possible it may help. As i say i still got ill when i gave up.

so there is more to it than immune suppression granted, (although how do we know those children were not immune suppressed in some way ? ) many forms of suppression possible, children apparently have less developed immune systems so im not sure that argues against this anyway. infact it may support the idea

but my point is, i got ill more often when under the influence of a possible immune suppression drug, i read somewhere pot lowered the immune response to swine flu helping avert a cytokine storm that has happened to a few swine flu victims, so if it can do that, then surely it must be lowering the immune defences, Which in the case of xmrv might be just a helping hand explaining why more immuno suppressed people will have it.
but further im suggesting it might help xmrv cause more damage. Is stress not something ME patients are told to avoid to reduce crashes. Does stress not help lower the effectivness of the immune system to fight viruses
im probably way off if so i apologies