German study finds xmrv

[RustyJ]

Starry Eyes, I thought I read a post that said the spread of HIV was hastened with excessive alcohol consumption. I also thought it was fairly well documented that XMRV spreads via the immune system (lymphatic system?). Hence an immune response to any virus may be enough to spread XMRV throughout the body. With children it may simply be EBV which is the triggering virus, it is very easily spread. If this is the case there may be little difference between so called sudden onset XMRV or slow buildup. The sudden onset symptoms people experience may be from a triggering virus such as EBV and not from XMRV at all. If this is the case, efforts to define or delineate XMRV by when it is sudden onset or not may be invalid.

 

[bluebell]

Law of parsimony

Retroviruses are nasty. You don't really need all these other factors to explain CFS/ME once it's shown that we have a retrovirus that causes illness in humans. It's kind of like going to the doctor to complain about a headache with a knife sticking out of your forehead, and saying, "yeah, the knife, I know...but I also ate some questionable egg salad yesterday in a restaurant that seemed to have a mold problem..." ;-). As others have pointed out, the numbers in this study support the idea that XMRV --> CFS, not CFS --> XMRV.

 

[free at last]

Out of my depth here so ill let the guys who understand these things more debate this But im reading and trying to understand what your all figuring out from this

. But just wanted to add something thats been bothering me, might make sense with this statement just posted. I recovered fairly well over the years with hardly any crashes like i used to get. But still get some weaker ones, with shorter duration 15 years into it ( but again pot after further intermitent use seems to make worse )
Hence my ideas of immune suppression making crashes more likely

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 Statement certainly fits in With What happened to my recovery. just had a crash recently after a few days of light 60s fun. Back to tea it seems

 

[free at last]

Retroviruses are nasty. You don't really need all these other factors to explain CFS/ME once it's shown that we have a retrovirus that causes illness in humans. It's kind of like going to the doctor to complain about a headache with a knife sticking out of your forehead, and saying, "yeah, the knife, I know...but I also ate some questionable egg salad yesterday in a restaurant that seemed to have a mold problem..." ;-). As others have pointed out, the numbers in this study support the idea that XMRV --> CFS, not CFS --> XMRV.

bluebell ive been doing this for years you know, they cant find a cause so ive looked far and wide for a reason, everything from ice cream to (i dont drink milk ) to chemicals in the enviroment. i suspect a lot have played this guessing game. want to know a cause so bad i guess, over to the experts. thats it im shush.probably not helping sorry everyone

 

[natasa778]

I don't think we should get too carried away though, we've not had anything published linking XMRV to CFS since the Science paper.

As Coffin said, a link won't be established until people start getting better on drugs that address that pathogen. That was how HIV was finally accepted as causing AIDS, nothing else.

 

[Gerwyn]

I read paper and I can't tell if they used the WPI method. If not, this shows that other methods can work.

they used a sample from lymphoid tissue in the lung.cultured the virus to amplify titre then used PCR to find the replicating virus.The virus lives in lymphoid tissue.The WPI isolated and looked in T and B cells but the principle is exactly the same.

They followed the instructions like any good scientist would. The prospect of airborne transfer adds a whole new dimension to this game. Edogenous retroviruses did not come from thin air.They were once infective exogenous viruses.They are thought to be our gene regulators.There is good evidence that they were responsible for changing our species by enabling the development of our neocortex in a twink of an eye in evolutionary terms.The Lord only knows what this one is capable of doing precisely because it is so close to an endogenous retrovirus.

 

[Gerwyn]

The cytokine signature produced in ME patients is consistent with the presence of a latent virus not a replicative one.XMRV is a latent virus.Active viruses are short term infections not chronic.The cytokine sigature in ME is found without any evidence of a co pathogen whatsover although co pathogens do occur.If co pathogens were involved ME would NEVER have this cytokine pattern without a co pathogen of some kind .XMRV is a retrovirus.If anything made us more susceptible to a retrovirus infectionthen we would almost certainly have the much more infective HIV virus and consequent AIDS

 

[RustyJ]

The cytokine signature produced in ME patients is consistent with the presence of a latent virus not a replicative one.XMRV is a latent virus.Active viruses are short term infections not chronic.The cytokine sigature in ME is found without any evidence of a co pathogen whatsover although co pathogens do occur.If co pathogens were involved ME would NEVER have this cytokine pattern without a co pathogen of some kind

Does this rule out XMRV being spread throughout the body through a mechanism triggered by another pathogen, eg a stimulated or compromised immune system.

 

[girlinthesnow]

Gerwyn,

I think I am right that WPI were able to culture XMRV and infect cells but did not find replicating virus in samples?

 

[Gerwyn]

Gerwyn,

I think I am right that WPI were able to culture XMRV and infect cells but did not find replicating virus in samples?

They found replicating XMRV in concentrated PMBc,s in fresh blood.You would expect this becauseof the presence of T and B cells which are lymphoid and replicating.you would not find it in dilute whole blood samples which were old as the Pmbcs are not replicating>the WPI got over this problem by concentrating the sample,activating then culturing before PCR

 

[Gerwyn]

Oliver Hohn is on this study and was also on the prostate cancer study with all negative results.

Hi Lans. yes he was this is what makes the ppositive study so significant

 

[parvofighter]

Aussie Rules

Alex, thanks so much for your cogent insights.

2-strikes make intuitive sense
It makes tremendous intuitive sense, and I'd be willing to bet that the 2-strike hypothesis will turn out to be "it".

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.

...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).

...I was at a conference in 1999 when de Meirleir discussed the risk of CFS being blood transmissable.

Two examples of that "Second Strike"
The following may interest you - one of what I suspect are many potential viral (and of course other) vectors for that "second strike":

1) FDA Recommends Screening Blood Products for Parvovirus B19; Parvovirus B19 can cause fever and fatigue (Note: and trigger ME/CFS)
From: Hemaware: The Bleeding Disorders Magazine; http://www.hemaware.org/story/fda-recommends-screening-blood-products-parvovirus-b19

The US Food and Drug Administration (FDA) issued a recommendation in July 2009 that makers of plasma-derived products, which include plasma-derived factor VIII and factor IX concentrates, begin screening for human parvovirus B19 by performing nucleic acid testing (NAT)... The FDA guidance recommends that NAT be done on source plasma and recovered plasma during the process of manufacturing plasma-derived products. NAT is already used routinely for detecting other viruses, such as hepatitis C and HIV, in plasma pools.

...Some patients, more commonly adolescents and adults, may suffer temporary swelling of the joints. But people whose immune systems are compromised by HIV, leukemia or other cancers or who have had an organ transplant can develop chronic anemia after exposure to parvovirus B19. (NOTE: And ME/CFS)

Approximately 5% to 10% of children younger than 5 have antibodies to the parvovirus; by the age of 60 approximately 90% of adults have anti-parvovirus antibodies. In people with hemophilia and other bleeding disorders who have been exposed to blood and plasma products, more than 90% have tested positive for antibodies to parvovirus B19 because of their additional risk of exposure through blood and plasma products.

The presence of parvovirus B19 in plasma products is well described, but it is notoriously hard to eliminate because it is a small,nonenveloped, single-stranded DNA virus. Its size makes it difficult to removeby filtration methods. A non-enveloped virus does not have a viral envelope surrounding it, which makes it resistant to the heat treatment and detergents often used to eliminate viruses during processing of blood products.
​

In short yes, it makes intuitive sense that one might find a heightened incidence of ME/CFS in patients receiving PVB19-contaminated blood products.
​

2) Transfusion-transmitted human parvovirus B19 infection in a thalassemic patient
From: Transfusion; http://www.researchgate.net/publica...ovirus_B19_infection_in_a_thalassemic_patient

A case of transfusion-transmitted HPV B19 infection in a 22-year-old female thalassemia major patient is described. She presented with an aplastic crisis; this was followed 1 week later by transitory heart failure and acute tricuspid incompetence... High-titer IgM anti-HPV and B19 DNA were also found in serum samples collected at the time of donation from one of the donors of the blood transfused before the onset of clinical symptoms...
​

CONCLUSION: This case documents the transmission of HPVB19 by the transfusion of 1 red cell unit and the occurrence of possible transient cardiac involvement in this infectious complication. (AND: did she go on to develop ME/CFS?)
​

In other words, I'd wager blood product transmission of ME/CFS is already happening. And I would argue that the repercussions of this postulated two-hit phenomenon extend far beyond the already-chilling potential connections with ME/CFS, GWS, autism, FM... to include viral cardiomyopathy - popularly called "idiopathic cardiomyopathy" in North America. The reason? While our cardiologists drive German-engineered cars, they don't typically conduct the necessary heart biopsy and tissue diagnostics (PCR, immunohistochemistry) which are recognized in German cardiology circles as the Gold Standard to establish active cardiac viral infection. Bottom line, I believe the ripple effects of XMRV might be far worse than we think - but this is a good thing as it opens hitherto closed doors to potentially more effective treatment.

A potential hiccup in the transfusion studies being developed in the US: If they only look for XMRV in the donor and recipient blood, they may be missing the "Second Strike" part of the equation. When investigating whether ME/CFS can be transmitted by blood products, shouldn't they look for BOTH strikes? Shouldn't they also look for ALL the opportunistic viruses which might hypothetically activate a latent XMRV infection? Too tired to finesse this - but this really needs to be followed up on. Thoughts anyone?

Some other thoughts:

• ME/CFS as occupational hazard. Yes, there is also evidence with at least this opportunistic infection (Parvovirus B19) that it targets especially caregivers/ professionals dealing with children under 6 years of age. An important consideration with PVB19 is that it is hopeless trying to prevent transmission (other than good hygiene) because by the time the most recognized symptom: the classic "Slapped Cheek" facial rash presents, the infectious stage has passed. Which is why you see these ruddy-cheeked preschoolers still at school.

In other words, even if an individual had a "regular" chance of contracting XMRV (say somewhere in the 2-6% range), their known and increased occupational risk of contracting PVB19 would arguably place them at higher risk of following the following pathway: XMRV+PVB19 = ME/CFS.​

• The French Connection: Remember the work of those French researchers early in the year, who identified XMRV's immunosuppressive virulence factor in the envelope? http://www.pnas.org/content/107/8/3782.abstract I believe this ties in neatly with what Dr Peterson was finding:

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....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.

I suspect there are additional mechanisms at play, but this envelope immunosuppressive factor alone (and the robustness of the Science work - being already from 3 institutions - and some of the papers in the pipeline) strenuously argue that XMRV will not be a "dead-end road". Further, I believe that as soon as the causal linkages are established, we will see political will developing to support proactive intervention: i.e. don't leave a smouldering XMRV infection untreated - even if you don't "yet" have symptoms. Of course the fact that many politicians at the height of their careers are concerned about prostate cancer will help keep XMRV on the radar screen.

Additionally, health economists can and should have a field day with this topic. Consider how many of us have been forced into unemployment with ME/CFS - and haven't paid taxes in decades. The do-nothing proposition carries massive costs that require "Total Cost" accounting.
​

• Will patients be treated as pariahs?: When considering the possibility of transmission through saliva etc, I am comforted by one thing especially. And that is the finding of XMRV in such a very significant proportion of normal controls. Do the math: if many school class sizes are around 25-30, one might have a reasonable expectation of having an XMRV-positive "healthy person" in every single class in America - and around the world. So frenetic attempts to minimize contacts with known XMRV patients may be rendered moot. That said, my fingers are crossed that we will be in the same boat as HIV patients: virus can be found in saliva - but not transmitted that way. That would make this whole "retroviral gift" easier to bear.

Finally, my read from Drs Holmberg, Mikovits, Ruscetti and Coffin etc. is that very soon we will know at least some of the pathology caused by XMRV. And given the linkage with the blood supply, cancers, (and hopefully the medical establishment here will clue into the cardiac side of things too), we may even have something which has been sorely missing for decades in this field: a sense of urgency among researchers and policy-makers. :Retro smile:​

 

[Rivotril]

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.

don't know if this was posted before (really think it was):


http://www.mefmaction.net/Portals/0/docs//Blood%20Transfusions%20and%20CFS.pdf

Blood Transfusion and Chronic Fatigue Syndrome
K. De Meirleir, P. De. Becker, I. Campine.

Presented at the Sydney February 1999 CFS Conference.

(...) In this group, 752 patients fulfilled the CDC criteria for CFS (Fuduka, 1994). Of
those CFS patients, 34 (4.5%) have a common factor in their past medical history
that immediately preceded the onset of their CFS. These patients had received a
blood transfusion a few days to a week prior to developing a flu-like syndrome
that later proved to be the acute onset of their CFS. (...)

 

[Rivotril]

http://www.prohealth.com/library/showarticle.cfm?libid=15356&utm_source=SiteTracking&utm_medium=SiteTracking&utm_campaign=home_LatestNews

 

[Megan]

- These researchers did not use the same techniques as the WPI.

Why do we think this paper used different methods to the WPI? I see thta one is looking at blood and the other at saliva but maybe the PCR is the same?

The original WPI science paper says:
"we isolated nucleic acids from PBMCs and assayed the samples for XMRV gag sequences by nested PCR (5, 6). Of the 101 CFS samples analyzed, 68 (67%) contained XMRV gag sequence"
If you look, reference no. 5 is to the Urisman paper that is also referenced in the German study under discussion in this thread. Reference no. 6 of the WPI paper is to their own supplementary materials that say "Nested RT-PCR for gag sequences was done as described (5)". Again in the supplement the Science article refers to, I assume, the PCR from the Urisman paper.

If you look up the original Urisman paper (free access - http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020025#ppat-0020025-sd002) and look at the supporting material download "Protocol S2. XMRV gag Nested RT-PCR", it describes a nested GAG PCR. Is this the one under discussion? Looks to me like this is the one used in the Fischer study we are discussing. I note also that Fischer is one of the authors listed the Urisman study.

Like others here this study looks like great news, but I am wondering if they have found it precisely because they used the same PCR test as the WPI? If so then it seems to me that this is not an issue of blood vs. saliva so much as demonstrating the difference between testing methods. If I have interpreted this correctly (I realise I might not have) then maybe this is more of a true replication study, in testing terms, than any of the others even though they were using saliva and not blood?

Are any of you more scientific types able to shed more light on these thoughts?

 

[Trooper]

Hiya

Nothing to contribute to the thread really, except to say thanks for making people, like me, aware of this study - it's big news.

Also thanks for all the comments, ideas and opinions expressed - some great food for thought!

Cheers : )

 

[garcia]

The 2-4% incidence in the general population is due to weak transmittability (sp), as it's a very low replicator. All these people will eventually become ME/CFS patients, but very slowly, so the incidence of ME/CFS doesn't exceed 0.5 - 1%. This happens by accruing damage from XMRV and opportunist infections.

This doesn't seem to be the case - e.g. the association with prostate cancer. There seems to be a significant population out there with XMRV who will never get ME/CFS.

 

[IamME]

This doesn't seem to be the case - e.g. the association with prostate cancer. There seems to be a significant population out there with XMRV who will never get ME/CFS.

Yeah I was going to include prostate cancer as well but left it out for simplcity :Retro wink: I don't know what the incidence of prostate cancer is in men with ME, it could be they die before getting ME. If people with XMRV die of old age without getting either ME or prostate cancer it could be they just died before they had time to fully manifest. When I said slowly I meant on average twenty years or more (less in a child suffer obviously; vertical transmission?). In this model XMRV is "stage 1" of ME or prostate cancer.

 

[eric_s]

Now it seems we have two German studies, one positive and one negative (Bannert). I think in both studies there were researchers involved from the RKI (Robert Koch Institut). Is there any paper available about the Bannert study?

What i'm thinking is this:
If those two studies have used different methods to try to find XMRV (i know one looked in blood and the other one in other substances, but i mean the PCR or whatever they've used), then it will probably only be a matter of time until the Bannert group repeats their study, this time using the more successful method.
This will be very interesting because it will more or less prove if the XMRV/CFS association is true or not. Now that there is another team in another part of the world that actually knows how to find XMRV, if they confirm the Science study's findings, then it will be clear enough, i think.

Does anyone know if the Bannert group could not find any XMRV at all? Or did they find the ~3% that would have to be there? If they couldn't find any, i think it's pretty safe to assume that they have used a different method compared to this latest study or did not work properly. On the other hand it seems a bit strange that people from the same institute work on studies parallely and don't exchange information about how to do it correctly. I'm really interested to see results of a study done at the RKI in PWCFS, using the techniques of this study, because i think the RKI is a good adress.

And referring to free at last and Stone, the same is to some degree true for me. When i got CFS (i never managed to pinpoint the exact date of onset because at that time i was of course not aware of the fact that this is to be taken seriously, so i did not think about it much) or around that time i was under a lot of stress, too. I was doing a lot of sports and always pushing myself to the limit. I was going through some sort of military training, which involved parachuting. I also liked to drink, smoke etc. at the weekends. Then i got some sort of infection, a bit like pneumonia, called tracheitis. Retrospectively, i could never say with certainty that this was were it started, but it would make sense.

 

[alex3619]

Hi Parvofighter

I agree with everything you said in your 7:03 PM post. I have also had the pariah discussion on other forums, as I am aware of at least one patient who has lost friends because of FEAR of XMRV - they weren't even diagnosed. The range of viruses that might be linked to CFS is quite long, and many may contribute specific symptoms. It has been mooted, but not demonstrated, that the core CFS symptoms might be XMRV, but the others are the coinfections - what you have determines how you feel. Best wishes, Alex

Bye
alex