How did XMRV enter humans?/Vaccines and XMRV

[Snow Leopard]

This topic has been on my mind since October '09, not least of which because my illness started straight after an immunisation... (as well as the article 'Endogenous retroviruses as potential hazards for vaccines' - Takayuki Miyazawa, which mentions CFS)

I guess if Mikovits is out of options reublishing, there is always this journal - the editor has MLV experience also. http://www.frontiersin.org/people/akioadachi/14796

 

[Jemal]

A vaccine could also be a trigger for XMRV of course. So you could already have been infected with XMRV and the immunisation triggered the immune system to start attacking XMRV as well, causing all kinds of symptoms.

 

[Carrigon]

With me, it was probably the forced polio vaccine when I was in college. After they forced me to get the shot, literally blackmailing me on it, telling me I would not be allowed back into any college anywhere unless I submitted, right after that, the entire year, my health went straight down till I was full blown CFIDS by that winter.

 

[August59]

Just an observation and it may have been brought up already? If xmrv proves to be the cause and if vaccines were considered to be the source, why wouldn't there be a much higher percentage of healthy controls testing positive? I'm guessing here, but I would think that at least 80% of the world population has received mutliple vaccinations. The USA percentage would be in the upper 90's for multiple vaccinations.

 

[Snow Leopard]

It's a probability thing - the probability of all the right conditions lining up. Even with regular viral infections, the probability of an individual virus achieving infection (after someone transferred the virus by sneezing for example), is vanishingly small. Yet viral infections happen.

An important point however: This evidence suggests that not all cases of CFS might be caused by XMRV (but you could have guessed that from VIP/Dx results for example and maybe even by common sense), and XMRV on its own might not be sufficient for CFS. In the same way that HIV doesn't automatically translate into AIDS (but often does), although the pathology is quite different so that example is not directly comparable.

 

[Bob]

From the conclusions:

In conclusion, the most likely mode of XMRV transmission points to mouse-derived
biological products, but it cannot formally be excluded that the virus was once transferred from feral mice to humans. The latter scenario is less likely as it would imply that a very rapid spread in the human population must have occurred to explain its presence on two continents. In this scenario, the extreme sequence similarity among XMRV genomes, both between and within individuals, would argue that the virus replicates at very low levels. Among the biological products, vaccines that were produced in mice or mouse cells are possible candidates that warrant further inspection. If XMRV was introduced in the human population through the use of biologicals, a background level of the virus in the human population, possibly varying with geography or age group, would be expected. Such a low level presence would then also explain the (absence of) detection of the virus in different studies, as well as its controversial association with disease.

We hope that this hypothesis will spur further discussion and help to resolve the many
remaining XMRV questions.

If it turns out that XMRV entered the human population via vaccines, then maybe this unique (?) mode of transmission into the human population, might be related to the lack of genetic variability that the recent Hue paper was investigating. Although, I think there is probably far more genetic variability than has yet been documented, as Judy has indicated that she has detected various strains of XMRV but hasn't published on it yet, as far as I'm aware, and Alter said that the pMRV's should be included when considering the genetic variability.

 

[SilverbladeTE]

Bob
*nods* (regarding lack of genetic variability)
that would make sense!
and also, the uter evil manipulation and abuse thrown at us:
pharma crops don't want ot lose money and vaccines are a $50 billion a year industry (And they keep throwing more of 'em at infant use DEMANDING they be used through government shills they've obviously bought off)

And governments are so arrogant they would rather let us rot than them lose face by being shown to have caused dreadful harm, or stop being so damn full of hubris, as they think "acceptable losses are ok, so we'll lie to the Public for their own good!" kind of thing.

 

[Mark]

Indeed, Bob, that's one of the points made in the Dutch paper I believe: that the supposed lack of genetic variability could equally well be explained by vaccine-transmission rather than by contamination. Somebody observed somewhere that the Hue paper could turn out to be a massive own goal, for precisely that reason. The vaccine theory seems to have gained massively more credibility recently, with some unexpected voices taking it much more seriously - perhaps it's slowly becoming possible to think the unthinkable?

One point that doesn't compute for me, about this whole genetic variability argument of Hue's, is that it's only based on an analysis of the very small number of isolates that have been found so far, at this very early stage in the understanding of XMRV - mostly in prostate cancer. How can it have the implications claimed, that the small number of XMRV isolates that have been sequenced are so similar, when we have no idea what other variants there may be knocking around as well that just haven't been detected yet because the primers don't match for those variants? Surely the similarity of the sequences isolated could just be a consequence of the testing methods used so far, the samples chosen for full sequencing, or the methods of isolation which might only pick up those particular specific strains? Something along those lines is surely at least a possibility?

And the other thing about it...I get the point that a live virus is expected to vary quite a bit - that's why Alter and Lo's PMLVs were taken as strong confirmation of the WPI - but hold on, weren't they saying back when Lo/Alter was published that (McClure) "let's be clear, this is a different virus" - and so those PMLV-like sequences can't have anything to do with it because they're different (though very, very similar)? So first we're told it can't be right because there's too much variation in the sequences found so far, and then we're told it can't be right because the sequences in one of the strains found are all too similar...sounds like another Catch-22 to me...

Re: Snow Leopard's important point, which is indeed a good point, touching on the co-factors: the reported findings of very high association with chronic lyme and mold sensitive patients are very suggestive to me. They suggest to me that one thing that XMRV is doing is enabling certain types of infections to remain chronic infections. So Lyme disease is well understood, Chronic Lyme isn't accepted though...but the point is that the XMRV is making a Lyme infection have chronic effects. Similarly, fungal infections are well understood, but permanent acquired mold sensitivity is also not accepted...but again the XMRV could be what makes the condition chronic. And the same could apply to certain types of viral infections: with XMRV knocking around, the body can never fully clear them. The potential mechanisms for this to happen seem so obvious and easy to imagine that it rather leaps off the page: if XMRV infects specific types of B or T cells, associated with specific types of antigens, perhaps because those antigens happen to active at the time of XMRV infection, then whenever your body tries to fight that particular type of infection, XMRV comes out to play.

How tedious that we've all been obliged to spend so much of our time and energy digging deep, deep, deep into tedious political arguments about theoretical contamination possibilities, instead of exploring the much more fascinating detail of how XMRV might work, and how it fits in with all the other things we know about this whole spectrum of diseases. I return to a year-old theme: if you tested a whole bunch of different conditions for XMRV through WPI, and checked out which ones were associated, and the detail of which types of patients were infected, then you'd learn an immense amount of clues about what it is and how it works from the overall pattern. Anybody could do that, very cheaply in research terms, by sending their samples to VIPdx (assuming they'd take them under those conditions - and nobody has said they refused to) - yet it's all been left to the WPI, so that they know so much more about the whole thing - the world is basically handing them a monopoly on this science. And you could get to the truth about CFS/XMRV reliably and quickly by methods like that, by challenging VIPdx labs to test your own samples blind, instead of doing your own contaminated studies and concluding that means the WPI are contaminated as well - which blatantly proves nothing and didn't get past anyone! Those who aren't asking the right questions in the right way, do rather suggest that they very much don't want to know the answers...

 

[alex3619]

Just an observation and it may have been brought up already? If xmrv proves to be the cause and if vaccines were considered to be the source, why wouldn't there be a much higher percentage of healthy controls testing positive? I'm guessing here, but I would think that at least 80% of the world population has received mutliple vaccinations. The USA percentage would be in the upper 90's for multiple vaccinations.

Hi August59, I have been thinking about this for days now. Consider that only about 1% of vaccines might be contaminated, to our current understanding. If we presume that we get roughly ten vaccines in our lifetimes (probably more, but hey, this is all guesswork at this point) and some develop resistance and fight it off, the number infected works out in the vicinity of what we see.

What will be very telling is if we look for xmrv in countries with very low vaccination rates and find almost no xmrv.

Bye
Alex

 

[Jemal]

It could have infected a vaccine that is no longer used. Maybe a vaccin people got decades ago. XMRV might now be spreading by other ways.

 

[alex3619]

It could have infected a vaccine that is no longer used. Maybe a vaccin people got decades ago. XMRV might now be spreading by other ways.

Right you are Jemal. There is speculation of a 1931 source, but we don't now how widely the infected cultures were used or if they are still in use. We need some investigation if this is proven true. Bye, Alex

 

[Bob]

Indeed, Bob, that's one of the points made in the Dutch paper I believe: that the supposed lack of genetic variability could equally well be explained by vaccine-transmission rather than by contamination. Somebody observed somewhere that the Hue paper could turn out to be a massive own goal, for precisely that reason. The vaccine theory seems to have gained massively more credibility recently, with some unexpected voices taking it much more seriously - perhaps it's slowly becoming possible to think the unthinkable?

Yes, the Hue paper has demonstrated the possibility of MLV contamination in cell lines, which gives enormous credibility to the vaccine contamination theory. After reading the Hue paper, it's hard to imagine that vaccines have never been contaminated with MLV's.

But now I really do worry about the vaccine theory becoming a mainstream theory as that will surely increase our enemies, and the funding that our enemies receive, a thousand-fold. Once the big pharma companies and governments see this theory gaining credibility, then goodness knows how many millions of dollars will be pumped into discrediting XMRV research, in order to avoid enormous legal claims.

One point that doesn't compute for me, about this whole genetic variability argument of Hue's, is that it's only based on an analysis of the very small number of isolates that have been found so far, at this very early stage in the understanding of XMRV - mostly in prostate cancer. How can it have the implications claimed, that the small number of XMRV isolates that have been sequenced are so similar, when we have no idea what other variants there may be knocking around as well that just haven't been detected yet because the primers don't match for those variants? Surely the similarity of the sequences isolated could just be a consequence of the testing methods used so far, the samples chosen for full sequencing, or the methods of isolation which might only pick up those particular specific strains? Something along those lines is surely at least a possibility?

It's very confusing because at the moment they seem to be looking to make primers more specific for XMRV, in order to avoid false positives in the form of MLV contamination, but is it the case that the more specific a primer is, the less likely it is to pick up on genetic variability?

And the other thing about it...I get the point that a live virus is expected to vary quite a bit - that's why Alter and Lo's PMLVs were taken as strong confirmation of the WPI - but hold on, weren't they saying back when Lo/Alter was published that (McClure) "let's be clear, this is a different virus" - and so those PMLV-like sequences can't have anything to do with it because they're different (though very, very similar)? So first we're told it can't be right because there's too much variation in the sequences found so far, and then we're told it can't be right because the sequences in one of the strains found are all too similar...sounds like another Catch-22 to me...

As far as I'm aware there's been relatively very little sequencing of XMRV so far, so there must be very little insight into the nature of the variability. And, like you say, Mark, once they do detect some genetic variability in human MRV's (i.e. PMRV), then it's dismissed by the deniers as a different virus who say that it's not relevant to XMRV research. Thankfully Alter recognises that XMRVs and PMRVs are all part of the same story.

How tedious that we've all been obliged to spend so much of our time and energy digging deep, deep, deep into tedious political arguments about theoretical contamination possibilities, instead of exploring the much more fascinating detail of how XMRV might work, and how it fits in with all the other things we know about this whole spectrum of diseases. I return to a year-old theme: if you tested a whole bunch of different conditions for XMRV through WPI, and checked out which ones were associated, and the detail of which types of patients were infected, then you'd learn an immense amount of clues about what it is and how it works from the overall pattern. Anybody could do that, very cheaply in research terms, by sending their samples to VIPdx (assuming they'd take them under those conditions - and nobody has said they refused to) - yet it's all been left to the WPI, so that they know so much more about the whole thing - the world is basically handing them a monopoly on this science. And you could get to the truth about CFS/XMRV reliably and quickly by methods like that, by challenging VIPdx labs to test your own samples blind, instead of doing your own contaminated studies and concluding that means the WPI are contaminated as well - which blatantly proves nothing and didn't get past anyone! Those who aren't asking the right questions in the right way, do rather suggest that they very much don't want to know the answers...

Well, let's hope that 2011 brings some big leaps forward for us, in terms of published positive studies. There's a lot of people working on XMRV/PMRV now, so what we need is some progress in terms of published positive studies. There must be some very significant papers in the pipeline by Singh, Alter & Lo, the Ruscettis etc etc.

 

[rwinsmom528]

Watch governments scramble to limit liability!

Our governemnt has already protected big pharma in that regard and has protected itself as well in that it is extremely hard to prove vaccine injury to get compensation from the government with their vaccine comensation program- mostly because docs won't acknowledge the connection between vaccines and vaccine injury even if it occurs within 24-48 hours of the vaccine.