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German study finds xmrv

Cort

Phoenix Rising Founder
Any betting people on here?

My bet that they are going to go in the direction of 'yes it is there but it does not do anything... only a passanger.'.

Then when CFS high incidence is confirmed they are going to stick to the line of 'pwc catch it because they are immune compromised. they are immune compromised because of stress and depression. they are depressed because they are somatising. somatisation causes immune suppresssion. xmrv is there but not pathogenic and should not be treated etc etc.


They will do their best and for sure, passenger virus will be the next line of defense. It'll be interesting. I'm sure that people are looking for XMRV in other diseases as we speak. If it shows up in say 10 or 20% of X disease and 75% of CFS patients how are they going to explain that? Even if it is a 'passenger virus' why would it have such higher prevalence in CFS? That would indicate some pretty nasty immune dysfunction wouldn't it?

Of course they will say....yes, they are deconditioned, their immune systems are crap because of that...but most of us aren't deconditiioned. I may not be 'conditioned' but I'm certainly not 'deconditioned'. I have a feeling that won't go far..[plus the retrovirologists don't give a fig about the cognitive behavioral therapists or Dr. Wessely or Peter White or whoever. Wessely is in his world and they're in theirs.

The retrovirologists want a new bug, they have lots of money, they have lots of tools, the infrastructure is there and they'll jump all over it and us once those positive studies start flooding in. Once they start finding XMRV the science will out; the heavy technology in the US will come to bear (as it is now) on XMRV and the little CBT crowd in the UK will scatter. It'll be like a big battleship turning its guns on a little frigate - kaboom!

All XMRV has to do is keep proving itself (still a question, of course) and the research community in the US and elsewhere will do the rest. This bad six months will be a blip on screen if those positive studies start rolling in. That's my expectation.
 

Cort

Phoenix Rising Founder
Mark - So anyway: given that the Germans have now found a background level of 3% or so, consistent with US and Japanese findings, the probability of the UK studies testing hundreds of samples - ME/CFS or otherwise - and finding no XMRV, is infinitesimally small.

If 3% of the population have XMRV, then at least 3% of ME/CFS patients should have it. Even if it's not associated with ME/CFS, they should still have found some XMRV in some of the samples. Even at 3%, with a few hundred samples, the chances of finding none at all are very, very small.

I would note that positive studies are much more powerful than negative studies. Its easier to miss XMRV than find it. I would think it would only take a few positive studies or even only one - if it was done in the right hands and done very rigorously - to turn the whole thing around.
 
G

Gerwyn

Guest
Hi Gerwyn. Ok, Ill bite, lets do as you suggest. The conundrum becomes:

Interpretation doesn't matter, only facts are important.
Facts require interpretation.

The point of the conundrum is still not changed, it is still the same message with the same implications, just a little less poetic. It is still a loop. It still teaches the same message. Interpretation and facts are interconnected. They CANNOT be separated. Facts can only be interpreted within a framework, but that framework could always be invalid and you have to go back to the facts for verification or modification. Science is based on this principle. A different framework can take the same facts and give a different conclusion. If someone comes up with a better framework, then the meaning will change and the old framework is often invalidated - but even if they are due to error or fraud, the facts remain unchanged, only their system theoretic interpretation changes.

By the way, this comes from systems theory not philosophy, although I stated it in phisosophical terms. Most philosophers dont seem to understand systems theory, or at least not the ones I have debated with.

The biopsychosocial people have their own theoretical framework - deeply flawed as far as I am concerned, but I think most of them actually believe in it. Under their framework they probably conclude the WPI research is dead, or about to be (and hence I think many will be shocked when this is sorted out). My framework in science is very different. I see the biochemistry as very compelling, it explains almost everything even if they haven't gotten around to formally expressing these explanations (scientists like to get some proof first, and dislike speculating). The explanation is so good that, like others on this list, if the WPI research were to be disproved I would want to start looking for another retrovirus. Same facts, different framework (interpretation), different conclusions. Different world views (theoretical frameworks) lead to many arguements, it is not just philosophical word games - which I agree can be a major problem, and politicians use these all the time, as do the biopsychosocial people. Indeed, their version of cognitive therapy is based on such word games. My earlier comment on buzzwords is grounded in this problem.

You are correct in saying that precision is important, if I interpret you accurately. The problem is that this is easy in theoretical physics, but as you progress to chemistry and then medicine it becomes more problematic. Psychiatry is only marginally less problematic than sociology, and as you move further from hard math the potential for problems to arise only increases. My point is that even if it sounds precise, one still needs to be carefull. It needs to be questioned. Ultimately, it needs to be grounded in the facts. Colour me a skeptic, at least of this variety. When one reads a scientific paper, and not an abstract which is often biased, everything can be questioned. According to Popper, science is more about disproof than proof. This is what is happening on these forums (questioning), and is a usefull way to enhance understanding.

You are also correct in stating that people need to understand the function of tools such as statistics. Even logic is deeply flawed, there is a formal logical disproof of logic. It is the translation from real world to math and back to the real world that catches people out, no matter how well educated or precise they are. There is a saying in semantics that later became a part of systems theory: the map is not the territory. This is why scientists need to go back to the real world, no matter how compelling the arguement, and test their hypotheses - or their statistics (which are, after all, only probability estimates).

I apologise if I am going into this too deep for many, or am too off topic. I could say a lot more, maybe even a small book, but this isn't the forum for it. I am happy to continue this debate, but it is probably better to do it via private email, should anyone be interested.
2
Bye
Alex

facts dont require interpretation that is the point,you can express an opinion that facts need interpeting but that opinion need not be objectively valid.The "conundrum" is the production of words used in an inappropiate context without any definition of meaning. Only absolute facts matter absolute facts by definition require no interpretation.Fact is a slippery word!
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi Tina,

I know what you mean about keeping notes. The moment I switch my train of thought the old thoughts are gone. :)

Regarding the virus, XMRV is a very well adapted virus. The evolutionary trend in viruses is to become both unseen to the immune system, and nonpathogenic. This keeps the host alive and spreading the virus, and does very little harm. It is new viruses, that cross the species gap, that tend to be severely pathogenic.

There is debate over whether the increase in CFS is due to dodgy definitions (it includes a lot of people who have other problems) but I still suspect you are right. Cheney noted a decade ago that CFS appears to be on an epidemic growth curve, but he couldn't be sure because of delays and problems in diagnosis. While I have commented before that 2/3 people in families with XRMV also have XMRV, this also means that 1/3 don't have it. I would really like to know why. Studying their genetics should be a priority.

Bye
Alex

I hate it on threads like this that are active. I read posts after mine that make me think of a comment, but by the time I get to reading them all, I have forgotten my comments. I need to keep a notebook next to me for when I read threads.

I do remember this thought. There is more CFS now than in years past. This is either change in lifestyle or infectious agent or change in environment. My point is, the increase does fit an XMRV is cause model.

Now, with all infectious agents, many get it but do not get sick. And some are immune. Think of FeLV, it has been around a long time. Few cats are immunized from it (mine isn't and neither was the one I had before). Yet it isn't killing off large percentage of cats. So even without a treatment or vaccine, we are not going to see "everyone" getting ill from XMRV. Just as we might have husbands (most of us) and I guess wives, that have not gotten sick, even though we have the virus. As I said, seems triggers may play a key role, and possibly genetics, although I am bearish on that line of thought.

Now, I got to go reread the posts to remind myself of the other comments I wanted to make.

Tina
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
financial imperatives

Hi Cort,

I think the comment I quote below is dead-on accurate. The biopsychosocial people have been feeding at the gravy train for decades, hogging all the funding. The retrovirologists are probably a much more powerfull group, much more respected. I don't think they will let go until they have answers. For once, vested interest may work for us. :)

Bye
Alex


The retrovirologists want a new bug, they have lots of money, they have lots of tools, the infrastructure is there and they'll jump all over it and us once those positive studies start flooding in. Once they start finding XMRV the science will out; the heavy technology in the US will come to bear (as it is now) on XMRV and the little CBT crowd in the UK will scatter. It'll be like a big battleship turning its guns on a little frigate - kaboom!
 

flybro

Senior Member
Messages
706
Location
pluto
Once they start finding XMRV the science will out; the heavy technology in the US will come to bear (as it is now) on XMRV and the little CBT crowd in the UK will scatter. It'll be like a big battleship turning its guns on a little frigate - kaboom!

this put in in mind of my brother playing with his toy soldiers and tanks, and the eternal kabooms that went with it.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
the problem with facts

Hi Gerwyn,

1 + 1 = 2 is a fact. In other mathematical frameworks, however, the answer is 11 or 10. I have even seen math that can prove that 0=1=infinity. Math is fact, because it is defined by a rigorous famework, but doesn't always translate to the real world. Did you know that much of modern electronics is based on the math of imaginary numbers?

When a researcher states they studied 250 CFS patients, it only makes sense when you understand who those patients were, what criteria were used, and what the confounding factors might be. In other words, you need a systems context. So the 250 patients is not a fact, its an observation (or observational hypothesis if you prefer) - it could be 3 CFS patients and 247 mistakes. Similarly, when one measures temperature in an experiment and get 25.1% degrees plus or minus 0.1, one is making an observation. Observations include observers, they introduce a complex human element. This is why we try to estimate the error factor. However there are so many possible confounding factors that we can never be really sure. What if one had brain or eye problems, or the thermometer was faulty, or the wrong figure was written down? What about the issue that temperature measure is only approximate, to one digit? What if there were extaneous factors that altered the temperature or its measurement, and you were not aware of them? How can a "fact" be anything other than absolute?

One solution, taken by systems theory, is that facts have context (in the broader not linguistic sense). Understanding this context gives you a handle on what the fact means. This may not be the only solution, but it is the only one I am happy with because it gives a handle to solving problems in complex domains. This does not deny an external objective reality, it acknowledges that our understanding of reality will forever be imperfect, and makes allowance for that. It also provides us with methodologies for creating consensus views of almost anything, but this takes lots of time and effort.

Science tries to get around this problem by emphasing repeated experiments by independent researchers, and by increasing the scale of the experiment (eg 25000 instead of 250 patients), in the hope that error and confounding factors can be minimized. Those versed in the scientific philosophy of Karl Popper also promote science as disproof. You can never be sure you are right, but you can always prove something is wrong. Science doesn't always work that well, which is why we are having so many debates about XMRV.

When I say "fact", other than in an abstact defined domain (eg math), I am aware that this is really just an "observation", and that the observation has context. A tip for understanding what people are saying when they make value judgements (good, bad, better, worse, etc) is that it strongly implies the criteria they are using for judgement. Understand the criteria, and you understand their judgement, and it allows you to respectfully disagree, because you have different criteria. This is why so many people have different views about the same "facts", although there are also issues around agendas.

Dont get hung up on the conundrum itself. It is only a teaching tool. It is designed to provoke thought and debate, and so enhance understanding - from the thought and debate, not the conundrum itself. Its my bad for introducing it, a hangover from my lecturing days. :ashamed:

Just to clarify, I am in no way put out that you are asking questions or making these points. Questions are always good.

Be careful with talking about meaning, it is a theoretical minefield. I spent years studying and defining and argueing about meaning in a post graduate setting, as part of my artificial intelligence research(AI = pragmatic application of meaning). It is not as simple or easy as most people like to think, and for most arguements there are dozens to hundreds of counter arguements. I have never seen an arguement, yet, that can trash the systems theoretic viewpoint, and I am a big fan of the work of Matura (who I met) and Varela. Every other framework is much more problematic. I can give many lectures on the theory of meaning, even now when I have forgotten most of it, but it is not a good topic for this thread. If you would like to take this to another thread, I am happy to do so, or continue this via email or messaging.

Bye
Alex

facts dont require interpretation that is the point,you can express an opinion that facts need interpeting but that opinion need not be objectively valid.The "conundrum" is the production of words used in an inappropiate context without any definition of meaning. Only absolute facts matter absolute facts by definition require no interpretation.Fact is a slippery word!
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
is XMRV just a reactivated virus?

H ladybugmandy

It is all about prevalence rates. It is certainly possible that this is just another reactivated virus, we have to wait on the science to be sure. The issue, with me, is that it explains so damned much that I use it as my working hypothesis. Now I also believe that CFS comes in different forms. Some of us wont have XMRV. I would definitely be thinking about similar mechanisms to XMRV, possibly a retrovirus, for most of these patients. although I am also aware that XMRV testing is so poor at the moment that false negative results are probably common.

However, I was a subject in a study on the prevalence of cotrisol binding globulin mutations in CFS. These mutations produce CFS-like symptoms by interfering with cortisol chemistry. If such mutations exist, I would put money on there being others. A possibilty was also raised a decade ago (in 2 studies) that many with CFS have undiagnosed phosphate diabetes (the inability to retain phosphate and so it is excreted). I don't know how that research panned out however, it may have been disproved, it is certainly being ignored. The point is that there may be many such disorders, all in small numbers and so not coming to the attention of researchers - another case of the CFS diagnosis being a too hard basket. The good news is that if XMRV+ patients are excluded from future CFS studies (being enrolled in XAND studies instead) then the XMRV- people may get the reseach they deserve and need. I know I will be supporting them, whether I am one of them or not.

CFS is probably mostly XMRV, some other pathogens, and an occasional rare genetic problem. We need more science to be sure.

Bye
Alex


if there people who are healthy and XMRV+, and more people who are immunocompromised and XMRV+, wouldnt that mean that XMRV is just another infection that can reactivate in people like HHV6 or EBV?

do you guys still think it is the cause of CFS?
 

Dr. Yes

Shame on You
Messages
868
if there people who are healthy and XMRV+, and more people who are immunocompromised and XMRV+, wouldnt that mean that XMRV is just another infection that can reactivate in people like HHV6 or EBV?

do you guys still think it is the cause of CFS?

Hi Ladybug,

The level of immunosuppression those transplant patients were undergoing would favor any virus. The fact that more of them were XMRV positive would only mean (unless they were more likely to get XMRV from receiving a transplant or more likely to have it from needing one) that XMRV replicates more easily when there isn't much of an immune response, like any other virus. That doesn't tell us anything for or against the likelihood that it causes ME/CFS.

[Btw HHV-6 and EBV haven't been ruled out as possible causes of ME/CFS either.. but the (little) evidence we have so far on XMRV looks better to me]
 

awol

Senior Member
Messages
417
That doesn't tell us anything for or against the likelihood that it causes ME/CFS.

Actually it might. If it is ONLY there in 10% of immune suppressed patients, but is there in at least 67% of ME/CFS that reinforces the case that it is a cause of ME/CFS and not just an opportunistic infection that happens to hit us because our immune systems are messed up.
 

parvofighter

Senior Member
Messages
440
Location
Canada
I think awol's got a point!

Dr Yes, I think awol might actually have a very lucid point. In response to the question of whether the immunosuppressed transplant patients' 10% or so XMRV rate has any significance for whether XMRV is causal in ME/CFS patients:
Actually it might (support causality of XMRV for ME/CFS). If it (XMRV) is ONLY there in 10% of immune suppressed patients, but is there in at least 67% of ME/CFS that reinforces the case that it is a cause of ME/CFS and not just an opportunistic infection that happens to hit us because our immune systems are messed up.
There is a simplicity in this response that makes a heck of a lot of sense to me. Consider how aggressively the immune systems of transplant patients are suppressed to prevent transplant rejection. It's immune armageddon. Would it be fair to simplify this by saying transplant patients are already at infinity in terms of immunosuppression - resulting from powerful immunosuppressive drugs - to prevent rejection. So how could ME/CFS be more immunosuppressed than transplant patients - if it's immunosuppression that predisposed ME/CFS patients to "opportunistic infection" by XMRV in the first place. Infinity plus one is still infinity.

So that leads to a very logical hypothesis that the 67% figure of XMRV in ME/CFS DOES suggest causality. Whaddaya think Dr Yes... Others?
 
K

Knackered

Guest
So that leads to a very logical hypothesis that the 67% figure of XMRV in ME/CFS DOES suggest causality. Whaddaya think Dr Yes... Others?

Personally I wouldn't use the term CFS, I'd either use ME or CCD CFS. The WPI are hitting 99% positive for xmrv with CCD CFS/ME, for CFS with misdiagnosis and Oxford criteria etc the percentages would be much lower.

Doesn't mean those of us who are XMRV negatives aren't physically ill though.
 

awol

Senior Member
Messages
417
Doesn't mean those of us who are XMRV negatives aren't physically ill though.

I agree. It might turn out that xmrv is A cause, not THE cause. That should by no means lead to the abandonment of the XMRV- among us to the psychobabblers. They will just have to renew the search.
 
K

Knackered

Guest
I agree. It might turn out that xmrv is A cause, not THE cause. That should by no means lead to the abandonment of the XMRV- among us to the psychobabblers. They will just have to renew the search.

It won't be A cause, it will be THE cause for a certain percentage of people who have been diagnosed with CFS.
 

Dr. Yes

Shame on You
Messages
868
Actually it might. If it is ONLY there in 10% of immune suppressed patients, but is there in at least 67% of ME/CFS that reinforces the case that it is a cause of ME/CFS and not just an opportunistic infection that happens to hit us because our immune systems are messed up.

Hi awol,

Yes, I should have been more clear.. I meant in itself this result doesn't tell us about XMRV's potential role in ME/CFS, i.e. it doesn't mean that it is more likely to be a passenger virus.

However, I'm not certain that we can make the jump to comparing this test group's numbers to the WPI's, and to conclude that this makes it less likely that it is a passenger virus; artificial immunosuppression is very different than certain 'natural' immune dysfunctions and opportunistic pathogen profiles can be different in these cases. Also, note that none of the 16 XMRV positive transplant patient samples in the German study were positive for any of the opportunistic viruses commonly seen in HIV or ascribed to ME/CFS (such as CMV and EBV). I am actually still intrigued by this result and wonder whether it suggests some tropism by XMRV towards the respiratory tract.

(I think that's the first time I used the word "intrigued" on this forum! Haven't used it since my last science-y job application..)

ETA - okay, just saw all the other posts! Parvo, my first impression when I read this study was the same as awol's, that if anything the low percentage suggested that XMRV was not a classic opportunist. But as I pointed out above, there are a lot of variables here. This study was in respiratory secretions, not in the blood; there is no evidence of most of the usual viral suspects in these transplant patients either (CMV, EBV, enteroviruses; they didnt look for HHV-6), so there isn't evidence to suggest that those are passenger viruses either; there is the possibility of respiratory tissue tropism by XMRV, which would not allow us to assume that what we are seeing here is a result of immunosuppression alone. [I forgot to mention that in my post to ladybugmandy.] Also, immunosuppression by drug therapy is a broad knockout of a lot of the immune response, but which pathogens take advantage of that is not merely a function of the weakness of the immune response but also of the ecology of pathogens within the host. Given a clean slate, a different ecology will emerge depending on what that patient has been exposed to and how those pathogens interrelate with the host and with each other. So I think the situation is too complicated for such a clear-cut conclusion.
 
G

Gerwyn

Guest
Hi awol,

Yes, I should have been more clear.. I meant in itself this result doesn't tell us about XMRV's potential role in ME/CFS, i.e. it doesn't mean that it is more likely to be a passenger virus.

However, I'm not certain that we can make the jump to comparing this test group's numbers to the WPI's, and to conclude that this makes it less likely that it is a passenger virus; artificial immunosuppression is very different than certain 'natural' immune dysfunctions and opportunistic pathogen profiles can be different in these cases. Also, note that none of the 16 XMRV positive transplant patient samples in the German study were positive for any of the opportunistic viruses commonly seen in HIV or ascribed to ME/CFS (such as CMV and EBV). I am actually still intrigued by this result and wonder whether it suggests some tropism by XMRV towards the respiratory tract.

(I think that's the first time I used the word "intrigued" on this forum! Haven't used it since my last science-y job application..)

ETA - okay, just saw all the other posts! Parvo, my first impression when I read this study was the same as awol's, that if anything the low percentage suggested that XMRV was not a classic opportunist. But as I pointed out above, there are a lot of variables here. This study was in respiratory secretions, not in the blood; there is no evidence of most of the usual viral suspects in these transplant patients either (CMV, EBV, enteroviruses; they didnt look for HHV-6), so there isn't evidence to suggest that those are passenger viruses either; there is the possibility of respiratory tissue tropism by XMRV, which would not allow us to assume that what we are seeing here is a result of immunosuppression alone. [I forgot to mention that in my post to ladybugmandy.] Also, immunosuppression by drug therapy is a broad knockout of a lot of the immune response, but which pathogens take advantage of that is not merely a function of the weakness of the immune response but also of the ecology of pathogens within the host as well. Given a clean slate, a different ecology will emerge depending on what that patient has been exposed to and how those pathogens interrelate with the host and with each other. So I think the situation is too complicated for such a clear-cut conclusion.

Hi doc Fred is struggling are the three amigos up to helping? I agree the broad knockout is the key point also the proximity of the secretions to lymphoid tissue where every other known MLV replicates.When the "hit" the blood they all stop replicating.Fascinating creatures!
 

natasa778

Senior Member
Messages
1,774
I agree. It might turn out that xmrv is A cause, not THE cause.

There could be other (gamma)retroviruses around that are not even 'discovered' yet...

then there is deFreitas virus, various other jump-species ones like avian leukosis viruse/s etc etc the list is endless... if xmrv is confirmed as etiological in cfs or any other disease, then really anything else, any other virus capable of similar biological effects should be a suspect in those who are xmrv negative.
 

Dr. Yes

Shame on You
Messages
868
Hi doc Fred is struggling are the three amigos up to helping? I agree the broad knockout is the key point also the proximity of the secretions to lymphoid tissue where every other known MLV replicates.When the "hit" the blood they all stop replicating.Fascinating creatures!

Hey G that last thought of yours just killed Larry, Curly AND Moe for the night. They gobbed out one last round of speculation before they died: How many total cells are in the kinds of samples used in the German study.. if not as many as there are white blood cells in the blood volumes used by WPI, then does that mean the virus really is more concentrated in respiratory tissue? Building on that speculation... Do the mucosa-associated lymphoid cells in the respiratory tract have to replicate faster than white blood cells? If so, would that explain the relatively lower concentrations of XMRV in the blood?
 

awol

Senior Member
Messages
417
Hi awol,

Yes, I should have been more clear.. I meant in itself this result doesn't tell us about XMRV's potential role in ME/CFS, i.e. it doesn't mean that it is more likely to be a passenger virus.

However, I'm not certain that we can make the jump to comparing this test group's numbers to the WPI's, and to conclude that this makes it less likely that it is a passenger virus; artificial immunosuppression is very different than certain 'natural' immune dysfunctions and opportunistic pathogen profiles can be different in these cases. Also, note that none of the 16 XMRV positive transplant patient samples in the German study were positive for any of the opportunistic viruses commonly seen in HIV or ascribed to ME/CFS (such as CMV and EBV). I am actually still intrigued by this result and wonder whether it suggests some tropism by XMRV towards the respiratory tract.

(I think that's the first time I used the word "intrigued" on this forum! Haven't used it since my last science-y job application..)

ETA - okay, just saw all the other posts! Parvo, my first impression when I read this study was the same as awol's, that if anything the low percentage suggested that XMRV was not a classic opportunist. But as I pointed out above, there are a lot of variables here. This study was in respiratory secretions, not in the blood; there is no evidence of most of the usual viral suspects in these transplant patients either (CMV, EBV, enteroviruses; they didnt look for HHV-6), so there isn't evidence to suggest that those are passenger viruses either; there is the possibility of respiratory tissue tropism by XMRV, which would not allow us to assume that what we are seeing here is a result of immunosuppression alone. [I forgot to mention that in my post to ladybugmandy.] Also, immunosuppression by drug therapy is a broad knockout of a lot of the immune response, but which pathogens take advantage of that is not merely a function of the weakness of the immune response but also of the ecology of pathogens within the host as well. Given a clean slate, a different ecology will emerge depending on what that patient has been exposed to and how those pathogens interrelate with the host and with each other. So I think the situation is too complicated for such a clear-cut conclusion.

I agree that the numbers are not definitive yet, so hard to say. I also agree that the low numbers in transplant patients does not PROVE that it is not a passenger virus in ME/CFS. However it does still support the case. Not enough on its own to delcare case closed.

As for tropism towards respiratory tract, if the crimson crescents turn out to be correlated (see other thread) there is certainly a reason to believe so!
 
G

Gerwyn

Guest
I agree that the numbers are not definitive yet, so hard to say. I also agree that the low numbers in transplant patients does not PROVE that it is not a passenger virus in ME/CFS. However it does still support the case. Not enough on its own to delcare case closed.

As for tropism towards respiratory tract, if the crimson crescents turn out to be correlated (see other thread) there is certainly a reason to believe so!

I think that the link between crimson crescents and mitochondrial dysfunction could be relevant.This is linked to hepatotoxicity and of course M.E. It could be related to prexisting XMRV and hypothetically explain the higher XMRV levels in this group

I wonder if there is any samples from the patients pre transplant