FDA and NIH confirm WPI XMRV findings (report of leaked presentation)

[alex3619]

Hi villagelife

If someone is worried about polyspecificity, with a little research this risk can be reduced. If it couldn't, then no vaccine or antibody test would be specific for anything. Its a risk, but a known one that researchers try to reduce. However, if it was picking up something else, it might be a different retrovirus and so should probably be treated anyway.

Bye
Alex

 

[Eric Johnson from I&I]

"If you attempt to make a specific antibody against XMRV almost surely you are going to pickup SFFV also which confirms what I have been saying about polyspecificity. Given that we know the human metagenomic microbiota contains a semi-infinite number of sequences, the chance that any antibody is only picking up one target (XMRV) is very small indeed."

This is very weak reasoning indeed. If the human flora led to serological false positives for XMRV, then why not for HIV, tuberculosis, and every other parasite in creation. As Alex says.

Not that serological false positives don't exist. They do. They are a particular problem in syphilis, but in general they are not a common problem at all. In general, sero-reactions are used throughout both medicine and research with an assumption of serological specificity - an assumption that is very rarely invalid. With monoclonal antibodies, which I believe have been used by WPI, cross-reactions are even more unlikely.

It's true that another closely-related virus might cross-react. In that case, we should then study that retrovirus, again as Alex says.

 

[Eric Johnson from I&I]

> Culture causes contamination

The solution is of course to run control samples - treating them exactly the same as the case samples in every way. If you do that, then if you contaminate the case samples you will also contaminate the control samples, and you will see no difference between cases and controls.

In practice it is difficult to be absolutely certain you did not introduce some hidden variable by treating cases and controls differently. However, you can be /pretty/ certain. You address the residual uncertainty by getting other lines of evidence, using multiple non-culture methods. Which of course is exactly what was done here from the very beginning, as we have known now for like 8 months.

Every method in the world is something less than divine. So you run 3 or 4 different methods in parallel. Thus, a 0.03 chance for error becomes a 0.03^3 chance for error, so to speak. And then, finally, just in case you are a complete idiot and don't even know it, you always publish your stuff and let other skilled people in this wide world find out whether they can also do the same experiments. Hopefully, if your work is important, enough other people try the experiments that you can be pretty sure at least some of them are skilled enough to pull it off (because making these things work is not always easy).

 

[bullybeef]

Hi Eric,

Are you Eric from Incline Village, and if so, would you mind me asking how many people have been tested in Incline Village, and how many were positive? I understand if you cannot say.

Thanks in advance BB

 

[Forbin]

I saw on another forum they have been talking about xmrv, there saying the antibody test might not be reliable,
One doctor has said,

"If you attempt to make a specific antibody against XMRV almost surely you are going to pickup SFFV also which confirms what I have been saying about polyspecificity. Given that we know the human metagenomic microbiota contains a semi-infinite number of sequences, the chance that any antibody is only picking up one target (XMRV) is very small indeed."


The doctor also said

Culture causes contamination and those are the flaws in WPI's validation procedure which need to be resolved, in order to more fully understand exactly what genomes WPI's test is actually locating in the CFS patients.

These are all worry points that he has made! I never would of thought of any of this.

I googled this and these two comments are actually a conflation of statements made by Dr. Frank Ruscceti and commentary made on them by Dr. Trevor Marshall at marshallprotocol.com.

The actually quotes, in which Marshall quotes Rucessti, are:

MARSHALL:
"At 06:00 Frank [Ruscetti] says 'If you attempt to make a specific antibody against XMRV almost surely you are going to pickup SFFV also' which confirms what I [Marshall] have been saying about polyspecificity. Given that we know the human metagenomic microbiota contains a semi-infinite number of sequences, the chance that any antibody is only picking up one target (XMRV) is very small indeed."

MARSHALL:
"Frank [Ruscetti] at 14:05 'Culture causes contamination.' Indeed. Agreed 100%. Then he [Ruscetti] goes on to explain how they isolated antibodies from goat blood. Sigh..."

MARSHALL:
"Those are the flaws in WPI's validation procedure which need to be resolved, IMO [?], in order to more fully understand exactly what genomes WPI's test is actually locating in the CFS patients."

http://www.marshallprotocol.com/view_topic.php?id=13461&forum_id=39&jump_to=197057

Combining the statements of these two men into that of a single unidentified "doctor" is going to be misleading at best (BTW, both men are Ph.D.'s and not M.D.'s).

Dr. Ruscetti actually says, "So then we tried to look at the plasma by different methods because everybody tells me that culture causes contamination." Dr. Ruscetti then goes on to describe the different methods he used to counter this potential criticism.

So, even in the original unaltered text, Dr. Marshall is himself cherry-picking a quote from Dr. Ruscetti (in which Ruscetti is himself quoting others).

 

[Sam Carter]

who was the Doctor, Van der Meer?

Professor Google tells me the quote comes from Dr. Trevor Marshall.

ETA: damn! Beaten to the draw by the nimble fingers of Forbin!

 

[usedtobeperkytina]

It is way too early to speculate on this. The only path of transmission proven is blood to blood transmission, and that has only been shown in the lab. Others have noted before that the CFS incidence pattern does not fit with an STD or respiratory pattern.

All of this makes me want to learn more about Hepatitis C. Any experts here? Hep C was originally thought to be an STD, and it is asymptomatic for years before liver damage begins. Now it is thought to be blood transmissible, and 20 years after its discovery there is still no vaccine. Dr. Michael Houghton, one of the discoverers of Hep C, is a new member of the CFSAC.

Jenny, I think that fact that it isn't showing up at a higher rate in sexual partners does not mean anything. This virus seems very dependent on other factors or triggers as to whether the person develops the illness (if in fact, this is the underlying cause). In the case of HTLV, only one in twenty or one in twenty-feve people with the virus get T-cell lymphoma. That leaves a large number getting the virus and never getting sick. This is also reflected in FeLV, with 3-5% of free roaming cats infected, although it can be much higher in groups. Many of them recover quickly from the initial infection.

But with XMRV, it may be there are folks that don't get sick, some get CFS, others get FM and still others get prostate cancer. Just because mates of CFs patients aren't getting CFS at a high rate, doesn't mean they may not have the virus and get another illness caused by XMRV.

Tina

 

[Forbin]

Professor Google tells me the quote comes from Dr. Trevor Marshall.

It's a combination of Dr. Marshall and Dr. Marshall quoting Dr. Ruscetti so as to seem to be the views of one "doctor." See above.

 

[ixchelkali]

Also, I may be wrong, but I thought that development of a vaccine was for treatment (perhaps both will be worked on, I know they have been working on one for HIV/AIDS for years without success but hey are still trying).

A vaccine would be for prevention. Too late for those who are already infected, I'm afraid. But Dr Coffin mentioned at the CFSAC last October that because XMRV doesn't mutate nearly as much as HIV it would be easier to develop a vaccine. That's the problem they've had with HIV, by the time they develop a vaccine it's mutated to a different form, so it's like trying to hit a moving target. I think he also said it would be harder to develop treatments, because XMRV doesn't replicate as quickly and treatments work on replicating virus.

At least that's how I remember it, but y'all have a good idea how good my memory is anymore.

 

[Eric Johnson from I&I]

bullybeef,
No, I'm a different guy. Sporadic case, not epidemic. By the way, do we know for sure that sporadic cases have been tested and show the same rates of XMRV positivity? I know I was wondering about that in the past but I forget whether I ever found out the anwer.

 

[Eric Johnson from I&I]

There is such a thing as a therapeutic vaccine for people already infected with something. But that doesn't mean a therapeutic vaccine will necessarily be possible when it comes to a given infection. From what I'm reading, the FeLV vaccine apparently has no therapeutic value, I'm afraid. And in practice I don't think there are a lot of therapeutic vaccines that have been very successful.

 

[alex3619]

Hi ixchelkali,

Traditionally vaccines are for prevention. However, in cases where the immune system is not finding the target, a vaccine is used to teach the immune system how to find the target (e.g. in cancer research).

One way to develop a target approach would be to isolate blood from patients, treat the immune cells with a vaccine etc, and then reinfuse them. This is all very theoretical at the moment, but I don't see why this technology couldn't work for viruses - its just that it has never been done. So a vaccine could be used to treat XMRV infection, by cranking up a specific immune response. This might get around many of XMRVs methods for hiding from the immune system. However, since this would be an entirely new application, don't expect to see it any time soon.

Remember that most vaccines target infectious agents that come and go. You don't give a vaccine to someone who has beaten the pathogen, because their immune system is already primed. For an infection that the immune system cannot properly target, this is likely to be a different proposition. I predict that we will see more and more use of vaccines to target ongoing long-term infections. This is not something I have particularly looked into, so I could be wrong and so I welcome comments.

Bye
Alex

A vaccine would be for prevention. Too late for those who are already infected, I'm afraid.

 

[taniaaust1]

I agree with you Shelley. My daughter received several required vaccines to enter college in the medical field and late that year received the Gardasil vaccine which we know caused her CFS symptoms. There are hundreds of "Guardasil Girls" with CFS-type symptoms, and many wih seizures. They received the vaccines (there are 3 of them) at young age. I think they maybe the link in between autistic children and some adults with CFS/GWS. If you want to see worldwide the issue with Guardasil, just search it out or check VAERS (the vaccine side-effects report). Of course not eveyone has problems, so there is something that is specific to these girls that causes them to react. There also have been over 60 deaths reported although only a couple have actually listed COD as complications from Guardasil (most are from heart failure, and this is at average age of 16!!!).

My daughter im postive has autism (im Asperger's) and she's NEVER had a vaccine in her life. She sleeps far more than most children too (could be due to the Austism thou??) but i do really worry that her need for more rest than others, may end up going onto into CFS. (i used to believe maybe vaccines and chemicals were solely responsible for Autism but in her case i know it isnt the case.. with my CFS and MCS..she never got exposed to chemicals as most children do).

Would she suddenly develop CFS with a vaccination??? I hope she never decides to try one.

The possible answer for it all... maybe XMRV (as it's found more in Autism too).

 

[justinreilly]

XMRV and DeFreitas RV: Causative or just associated with ME?

Here's part 2 of my assessment that XMRV and DeFreitas RV are probably causative of ME:

note I am a layperson, sorry if there are any errors.

A couple of other things occurred to me on this question that point toward causation (there are others in addition I won't mention). Bear with me!

There are four recognized human retroviruses and each are linked to some extent with severe life-long or fatal neurological and immune disease. HIV causes AIDS. XMRV (the virus in question) is linked so far with ME and aggressive prostate cancer; HTLV I causes T cell lymphoma, leukemia and Tropical Spinal Paralysis; HTLV II has been tentatively linked to lymphoma (though this HTLV II link is not widely accepted; I don't know enough about this to comment).

The M in XMRV stands for Murine (ie mouse) Leukemia Virus which causes leukemia, lymphoma and neurological disease in mice. RV stands for 'related virus'. XMRV mutated out of MLV.

There are other MRV's that cause lymphoma in both mice and the other species they infect.

XMRV switches on a gene that effects mitochondria (the energy turbine of all cells). Mitochondrial damage is clearly established in ME and would explain the profound exhaustion and multi-organ nature of ME.

The seperate DeFreitas retrovirus discovered in ME in 1991 was electronmicrographed budding (rupturing) out of damaged mitochondria. This was the first time any virus was ever shown in an animal (including human) mitochondrion.

Thus it has not been proven that XMRV and DeFreitas retrovirus are causative of ME, but much compelling circumstantial evidence points that way.

Here's an email i sent my dad today stating what i think the significance of the NIH and FDA findings are. He had asked me if there was a causal association shown. (he worked long ago as a lawyer at FDA)

I wrote here that 9 of approx 200 got lymphoma, now i'm remembering i also heard the figure of 19, does anyone know? (pls PM me as well as posting thx).

Dad,

There's just a strong association, no direct proof of causation. how strong an association at FDA and NIH we don't know yet- will have to wait for the paper to be published (at least as strong 67% and sounds like stronger) WPI, CC and NCI published 67% using four methods but later found 98% by adding a fifth (presented at conferences but unpublished as yet).

I'd say the chance the most important cause of ME is retrovirus(es) (or very similar viruses) is 99%. There is no other plausible way to explain what I call the curious case of the woman from South Africa who transmitted Burkit's lymphoma to her four relatives in the US ca. 1982 all living in different parts of the US. Burkit's clusters in Africa, but there were only about 10 cases per year in the US at that point. So far 9 out of 200 of Dr. Peterson's patients in Nevada have died of Burkit's or the related (and also exceedingly rare) mantle cell lymphoma. He was able to culture XMRV from 20 year old mantle cells from one of his deceased patients and was able to get it to infect a seperate cell line! AIDS is the only other cause of these vanishingly rare lymphomas.

Thus the chance of catching Burtkit's in the early 1980's was about 30 million to one, but if you have ME (or AIDS) it's about 20 to one. There is no plausible way to explain this except that the retroviruses associated with ME cause the lymphoma and if they are pathogenic enough to cause fatal lymphoma, they are pathogenic enough to cause ME which presents as a classic retroviral neuro-immune disease.

AIDS is also the only other significant cause of the devastating HHV-6 infections that are common in ME patients. etc. etc.

XMRV and DeFreitas retrovirus probably work in concert (perhaps with other retroviruses and HHV6 etc.) but even if XMRV isn't the only cause, it most probably contributes very significantly to the illness burden and using HIV drugs on it will almost surely result in a significant reduction in illness burden, ie an effective treatment.

the main point is CDC, NIH and the UK govt will have to start funding this and stop persecuting us. this is the main reason we are so excited.

look forward to seeing you.

J


Justin Reilly



To: justinreilly
Subject: Re: XMRV in ME Confirmed by both NIH and FDA!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!
Date: Thu, 24 Jun 2010 10:39:10 -0400
From:

Hello Justin -

I read the article about the independent FDA findings. Question: Does the presence of the retrovirus indicate the cause of ME or a commonality among ME patients? If the latter, I gather much more needs to be done, but at least the investigators have a much better lead.

Love,

Dad

 

[SeaShel]

You don't give a vaccine to someone who has beaten the pathogen, because their immune system is already primed.
Bye
Alex

Hi again Alex -

I didn't clarify, but that's what I meant by being given an unnecessary measles vaccine. I had the measles as a child. My mom wrote all my childhood illnesses on my birth certificate. I remember having them. When I was pregnant with my only child, I was told I did not have the antibodies. They "made" me have the vaccine before I left the hospital after giving birth. I did not know I could refuse.

Six weeks later I was insanely ill for a solid month. High fever (spiked to 107), excruciating unrelenting headache, chills, aches, nausea, etc etc etc. In the early years of being ill with cfids, I talked to more than a handful of women on the net that had the exact same experience after a measles vaccine (various parts of the country).

FWIW

Shelley

 

[taniaaust1]

bullybeef,
No, I'm a different guy. Sporadic case, not epidemic. By the way, do we know for sure that sporadic cases have been tested and show the same rates of XMRV positivity? I know I was wondering about that in the past but I forget whether I ever found out the anwer.

That original study had mostly sporadic cases in it

"We did not state in Lisbon (7) or elsewhere that the samples analyzed in (1) were only from patients from documented outbreaks of CFS, nor did we state that the 101 patients described in (1) exhibited all the immunological abnormalities described in our Lisbon conference presentation. In fact, only 25 samples in (1) came from patients identified during the 1984 to 1988 CFS outbreak in Incline Village, Nevada. The remaining 76 samples included patients with sporadic cases from 12 U.S. states and Canada, including California, New York, North Carolina, Wisconsin, Michigan, Oregon, New Mexico, New Jersey, North Dakota, Texas, and Florida. " http://www.sciencemag.org/cgi/content/full/328/5980/825-d

 

[Eric Johnson from I&I]

thanks a lot

 

[alex3619]

Hi Shelley

I can partially relate. I had measles when I was seven, and then measles encephalitis (hey, thats also ME!). My GP was worried that I would get meningitis but I wasn't hospitalized, and was unconscious for over a week, except for a few minutes every now and then that I could be woken up. I have never been right since (this was in 1968), I was chronically tired with other CFS like symptoms appearing in my teens. In my twenties it cranked up from mild to moderate, then in 1985 I had a year with one flu after another, all year long. From 1992 I was on a downhill slide which reached its nadir in 96 and 97. Then I slowly started to recover.

I think measles, like hep B, may be a special case in terms of risk factor for developing CFS - both the disease and the vaccine are risky.

If your immune system was already primed by measles, and you had another vaccine, you could have had an unusually severe immune response. We know from the Dubbo study that this is a major risk factor for triggering CFS. XMRV would also love it. What you describe is not surprising to me.

Bye
Alex

Hi again Alex -Six weeks later I was insanely ill for a solid month. High fever (spiked to 107), excruciating unrelenting headache, chills, aches, nausea, etc etc etc. In the early years of being ill with cfids, I talked to more than a handful of women on the net that had the exact same experience after a measles vaccine (various parts of the country).
Shelley

 

[SunnyGal]

Sunnygal,

I am XMRV+ and had no physical or emotional stress leading up to my acute onset. This means for some of us, that cortisol may have been low or normal. My cortisol is low now and there is no evidence that it was ever high. No emotional stress that would have raised it.

A virus came out of the blue, hit me and I have never been the same. Arguing about a hypothetical high cortisol may be pointless when the facts don't support it.

If I can get ill with this virus with no obvious trigger then maybe others can.

You're completely missing the point that this virus you got out of the blue would cause your cortisol to go high. As I said, it's not only emotional stresses that cause cortisol to go high but also physical stresses such as an infection.

I'm not arguing about hypothetical high cortisol. It's simply a fact that infections cause cortisol to go high. That's how the body works. In the initial stages of an infection the body raises cortisol levels to deal with the infection. Over time, if the infection isn't cleared the adrenals become depleted and are unable to continue producing a high level of cortisol and then cortisol goes below normal levels. Nothing hypothetical about this fact. And as cortisol is a trigger for XMRV I don't see any argument for why you may not have had high cortisol at the onset of your illness.

 

[SunnyGal]

I agree ukxmrv+,

My 2 children got ill completely out of the blue with acute onset, never having been ill children before that, no undue stress etc. It seems a coinsidence that they both got ill at age 8.5yrs.
I got ill after them both, mine could of been helped along by stress of course, having to children with me/cfs is very stressful, although i to had an acute onset after a flu virus.

Please, people need to keep in mind that stress on the body doens't mean only emotional stress. An infection is a physical stress to the body which raises cortisol levels just as emotional stress does. So, children may not have any emtional stress causing elevated cortisol levels, but the early stages of an infection will also cause elevated levels of cortisol.