The Race to Retract Lombardi 2009...

[RustyJ]

Thanks, I had not seen that thread.

IF there are HGRVs in ME, they are unlikely in the MLV family as that has been thoroughly tested. So that might require novel sequences be discovered. But that still would require a transmission vector that defies the epidemiology of ME/CFS, unless the virus is nearly ubiquitous. Will be interesting to see if anybody finds reproducible evidence.

Hi Kurt, I wonder if the lab workers who are worried about infection now think HGRV have been thoroughly tested? I wonder how you can be so confident when they've only just realised the extent of contamination in multiple cell lines by x and pMLVs etc. To me this suggests they know next to nothing about them. When I see a poster with supposed experience in retrovirology saying there is no known retrovirus that is aerosolized, then I really wonder.

One thing is overriding in the comments of the non-patient HGRV naysayers: they assume a HGRV infection is non-pathogenic or causes a minor illness. This underlies everything. If they believed ME was serious you can bet potential transmission would be considered a lot more seriously.

Furthermore, I cannot understand the logic of saying HGRVs are dead, ad nauseum. What are you trying to achieve? What is the driving imperative here? Why do you feel it is necessary to step in to every discussion on HGRVs with this sort of pronouncement? Others have asked the same question, but I have yet to see you answer this.

I will keep asking this in my posts, and I think others should ask also.

 

[kurt]

Hi Kurt, I have said this many times, on many threads, the retroviral theory EXACTLY matches the epidemiology, its a PERFECT match. Its why the hypothesis is so compelling. I am not going to bother reiterating, again, why this is so. Claims to the contrary are based on simplistic viral, not retroviral, models. Bye, Alex

Well, I guess we disagree then, because I think blood-borne retrovirus by definition is a disease transferred by sexual contact, sharing needles by intravenous drug users, or vertical transmission (mother to child from breast milk generally). That is a very well-known epidemiology for HIV and HTLV, as well as a host of animal retrovirus diseases including MLVs and probably other gamma forms. ME/CFS on the other hand occurs in outbreaks among large, definitely non-conjugal, populations, within a short timeframe, such as during a flu-like illness outbreak. ME/CFS also occurs randomly in smaller clusters, in families, or in individuals. Long-term sexual partners of ME/CFS patients do sometimes get sick as well, but more often do not. A small but stable percent of post-viral patients go on to develop ME/CFS after EBV, parvo, Lyme, and probably others. I believe this puts ME/CFS in a category of genetic precondition plus air-borne or water-borne trigger pathogens.

Yes, you have said before that the retrovirus may have become universal through some unknown mechanism, such as vaccine contamination, and that we might just have unlucky genetics. That would be consistent with genetic precondition plus post-viral infection. But that theory has an up-hill battle because there have been outbreaks of ME/CFS since ancient times, by many accounts. Most recently during the Crimean war, the US Civil War, WW I, in the 1930s, the 1950s, and the 1980s. In the case of XMRV, that virus may be a lab creation from the 1990s, so unless it is a time-traveller, or the virology field has this all wrong, I think this idea would be a fringe theory. That said, sometimes fringe theories turn out correct, but I think in this case it is long odds.

Of course there might also be a novel transmission mechanism, but that would be huge if true, as it would apply to a host of retroviruses, and I have not heard any real evidence for that idea, just postulate. In fact there have been searches for novel transmission methods, I remember reading a study of ticks and retrovirus transmission a few years ago, I believe conducted in Africa to see if HIV spread by ticks, but if my memory serves there were enzymes in ticks that de-activated the retrovirus.

Hi Kurt, I wonder if the lab workers who are worried about infection now think HGRV have been thoroughly tested? I wonder how you can be so confident when they've only just realised the extent of contamination in multiple cell lines by x and pMLVs etc. To me this suggests they know next to nothing about them. When I see a poster with supposed experience in retrovirology saying there is no known retrovirus that is aerosolized, then I really wonder.

One thing is overriding in the comments of the non-patient HGRV naysayers: they assume a HGRV infection is non-pathogenic or causes a minor illness. This underlies everything. If they believed ME was serious you can bet potential transmission would be considered a lot more seriously.

Furthermore, I cannot understand the logic of saying HGRVs are dead, ad nauseum. What are you trying to achieve? What is the driving imperative here? Why do you feel it is necessary to step in to every discussion on HGRVs with this sort of pronouncement? Others have asked the same question, but I have yet to see you answer this.

I will keep asking this in my posts, and I think others should ask also.

I've never said I have retrovirus experience, I was an experimental researcher in another field (maybe you were referring to someone else?). I don't remember commenting about the 'unknown HGRV' hypothesis, but have commented that MLVs have been conclusively shown to not be present in ME/CFS patient blood, as multiple studies have tested the conserved portion of the genome that must be present for any MLV (WPI did not test that gene, other labs did).

So you think I am a 'nay-sayer'? What does that mean anyway? Just an oppositional-defiant type of person? Someone who disbelieves ME? That is simply false. If there were good evidence for MLVs, I would be supporting the idea. Also, you implied that if someone thinks ME is serious they would take potential HGRV transmission in labs more seriously. I think that sounds very authoritative, as if you know for certain ME is caused by an HGRV. Do you know that?

 

[barbc56]

At one point JM did say in a presentation (I believe in 2010) that they often had to run patient samples several times in order to get positive results. There are indications the control groups used in the Science study may have been tested at different times or in some other way differently than the patient samples. That is what I expect the Science investigation is most interested in, because realistically, if WPI could not replicate with the BWG study, there has to be an alternate explanation for the original PCR results. If the patient and control samples were run differently, then the whole paper is likely invalidated and should be retracted.

This brings up another point. If the WPI had to test patient samples several times to get a positive that means that each time the sample was tested, the chances are higher that contamination could occur.

I think you are probably right about where the science investigation is focusing.

I keep saying this. Time will tell.

 

[alex3619]

Well, I guess we disagree then, because I think blood-borne retrovirus by definition is a disease transferred by sexual contact, sharing needles by intravenous drug users, or vertical transmission (mother to child from breast milk generally). That is a very well-known epidemiology for HIV and HTLV, as well as a host of animal retrovirus diseases including MLVs and probably other gamma forms. ME/CFS on the other hand occurs in outbreaks among large, definitely non-conjugal, populations, within a short timeframe, such as during a flu-like illness outbreak. ME/CFS also occurs randomly in smaller clusters, in families, or in individuals. Long-term sexual partners of ME/CFS patients do sometimes get sick as well, but more often do not. A small but stable percent of post-viral patients go on to develop ME/CFS after EBV, parvo, Lyme, and probably others. I believe this puts ME/CFS in a category of genetic precondition plus air-borne or water-borne trigger pathogens.

Yes, you have said before that the retrovirus may have become universal through some unknown mechanism, such as vaccine contamination, and that we might just have unlucky genetics. That would be consistent with genetic precondition plus post-viral infection. But that theory has an up-hill battle because there have been outbreaks of ME/CFS since ancient times, by many accounts. Most recently during the Crimean war, the US Civil War, WW I, in the 1930s, the 1950s, and the 1980s. In the case of XMRV, that virus may be a lab creation from the 1990s, so unless it is a time-traveller, or the virology field has this all wrong, I think this idea would be a fringe theory. That said, sometimes fringe theories turn out correct, but I think in this case it is long odds.

Of course there might also be a novel transmission mechanism, but that would be huge if true, as it would apply to a host of retroviruses, and I have not heard any real evidence for that idea, just postulate. In fact there have been searches for novel transmission methods, I remember reading a study of ticks and retrovirus transmission a few years ago, I believe conducted in Africa to see if HIV spread by ticks, but if my memory serves there were enzymes in ticks that de-activated the retrovirus.

Hi Kurt, in 1955 it was shown ME is blood transmissable here in Australia although I have yet to get hold of the paper - I think it involved finding the same lesions in the brain and spine of monkeys some time after infusion. It was quoted several times after that. We also know many patients get sick after blood transfusions - around 5%. A retrovirus can not only cause similar pathology to that found in ME and CFS, it has a slow incubation period. MLLVs are likely to have a much slower incubation period than HIV, and it can take 20 years for someone to get AIDS (not usually perhaps, but its known). Every person could have contracted the retrovirus long before an epidemic, the epidemic was simply a confluence of factors that combined to trigger a retroviral outbreak in people already infected. The incubation period thus matches the coinfection that triggered the retrovirus. The retrovirus could even be passed down generation after generation, awaiting a trigger. Its spread in the population is likely to be a patchwork, not ubiquitous.

MLLVs have been around for many millions of years. Thats way longer than the known or suspected history of ME and CFS. They infect many different vertebrates, from birds to gibbons, cats and koalas. Humans would have come into contact with them millions of times, if not billions of times. We have very strong antiretroviral defences against them .... why have we such strong defences? The most plausible explanation is that we have been infected before, and it was devastating, causing a huge evolutionary advance in resistance (not immunity). Is every outbreak of ME or CFS is the same retrovirus? There are many strains of MLLVs out there. It is also possible that some, most or all outbreaks are not MLLVs at all, it could be another retrovirus.

The claim that XMRV arose as a lab recombination event in the early 90s is an hypothesis, several studies found it or something like it in the 80s that have been commented on since several times. This hypothesis is accepted far too readily. Even if its correct that recombination created the virus in the lab, pure chance (as I have discussed repeatedly elsewhere) could have created it millions of times in the natural population last century alone. So what if it appeared in a lab culture? They also did not rule out that the virus contaminated the culture. It does that, quite readily as it turns out. If the virus was around, it had a much higher probability of contaminating the culture than a chance recombination event. The recombination event is actually a much more unlikely hypothesis. Please note that I am not saying I know they are wrong, only that we should be sceptical.

The Lipkin study is the final world on XMRV-like MLV association as far as I am concerned. We wont know to a high degree of certainty until then. Even then it does not rule out the existence of an entirely different retrovirus, or even endogenous retrovirus reactivation via some mechanism. Nagalase is often found in patients, and it can come from a retroviral infection, though thats not the only cause. I think there were reports of isolated findings of reverse transcriptase, but I don't think its ever been systematically followed up. If it was followed up an d showed very high prevalence of reverse transcriptase in patients, it would clinch it in my view. We know of no other cause for reverse transcriptase.

I am not saying my model discussed here is correct, only that it fits the facts. I am still completely open to an autoimmune/regulatory problem as the cause, it was where I started in the 90s and it still makes sense. The Rituximab study unfortunately could be either immune or viral, as B cells can be affected by viruses, retroviruses or defects in immune regulation. It could even be due to an unintended side effect of Rituximab, not the B cell depletion at all. This is early days in the research.

To me one of the great questions is: why is there such a high viral tissue load, especially in the gut (but also muscle, including heart muscle)? What causes this? When we know the answer to that, I think we may be close to cracking the origins of ME and CFS. One of my hypotheses, a variant of something I said years ago, about low NK cell function is that it may be deliberate. At some point with a high viral load the body might have started attacking gut or heart, and the immune system was suppressed automatically. in other words, its a survival mechanism. Against this we of course have the issue that some patients with low NK cell cytotoxicity (and lets not forget T cell cytotoxicity is down too) have had the cytotoxicity restored and have not dropped dead, so I am not completely happy with this hypothesis.

The data is looking more and more like there are at least two types of CFS or ME. It is also possible this is subgroups due to genetics or some other factor. I would be interested to know if patients selected from specific outbreaks did not exhibit such subgroups.

Bye
Alex

 

[RustyJ]

I've never said I have retrovirus experience, I was an experimental researcher in another field (maybe you were referring to someone else?). I don't remember commenting about the 'unknown HGRV' hypothesis, but have commented that MLVs have been conclusively shown to not be present in ME/CFS patient blood, as multiple studies have tested the conserved portion of the genome that must be present for any MLV (WPI did not test that gene, other labs did).

So you think I am a 'nay-sayer'? What does that mean anyway? Just an oppositional-defiant type of person? Someone who disbelieves ME? That is simply false. If there were good evidence for MLVs, I would be supporting the idea. Also, you implied that if someone thinks ME is serious they would take potential HGRV transmission in labs more seriously. I think that sounds very authoritative, as if you know for certain ME is caused by an HGRV. Do you know that?

Not sure how you came to this response. My comments were directed at what you said, not you personally. I didn't of course mean you were a retrovirologist (though you have at times grandstanded the fact that you have often been privy to information from those circles), nor did I at any stage infer you did not have ME. Nor has your response addressed the question I was asking. Simply saying 'that the evidence is not there' is not a good enough reason, as surely you must acknowledge you are not really in a position to fully appreciate the evidence.

It's not a major secret that many of those posters (not all, and not you) who have joined the anti HGRV side of the debate had a less than sympathetic view of ME and certainly it could be argued that the CDC has perpetuated this view over the decades.

By now I don't think there are many on this forum who don't know you are against HGRVsl. I mean how many times, on how many threads is it really necessary for you to tell us that you don't believe in HGRVs? If people who are interested in HGRVs are discussing posts, why is it necessary for you to join the debate when it is only to make a negative comment or to reiterate a point you have made before. I can see how this sort of behavior could make posters wishing to discuss HGRVs a little aggressive.

Your final comment about the finality of HGRVs and ME typifies how some of your posts can polarise members. You appear to know/believe for certain that HGRVs are dead, whereas I disagree. Now what this means is that I don't think they are dead, not that I know for certain ME patients have HGRVs. There is a world of difference. Your argument resonates with the closing statments of those negative studies that trumpeted HGRVs are dead. Surely you can see this distinction.

 

[Bob]

Hi Kurt, in 1955 it was shown ME is blood transmissable here in Australia although I have yet to get hold of the paper - I think it involved finding the same lesions in the brain and spine of monkeys some time after infusion. It was quoted several times after that.

Yes, I believe that they injected monkeys with the blood of ME patients, and then later carried out a post-mortem examination of the monkeys' tissues and found tissue damage. I think this was years ago wasn't it, so it was a study of 'ME' patients, before 'CFS' existed?

We also know many patients get sick after blood transfusions - around 5%. A retrovirus can not only cause similar pathology to that found in ME and CFS, it has a slow incubation period. MLLVs are likely to have a much slower incubation period than HIV, and it can take 20 years for someone to get AIDS (not usually perhaps, but its known).

With HTLV, I believe that only about 5% (I can't remember the exact amount) of people who are infected actually get ill over their life time.

Every person could have contracted the retrovirus long before an epidemic, the epidemic was simply a confluence of factors that combined to trigger a retroviral outbreak in people already infected. The incubation period thus matches the coinfection that triggered the retrovirus. The retrovirus could even be passed down generation after generation, awaiting a trigger. Its spread in the population is likely to be a patchwork, not ubiquitous.

There could be some unpredicted method of transmission for HGRVs (if they exist), such as a retrovirus contaminant in a batch of vaccines.
So maybe there is a possibility that the outbreak areas were exposed to these contaminated vaccines many years before they became ill, and then they only became ill years later when exposed to a trigger event.
I'm not saying this is likely, but it does seem a hypothetical possibility.

The claim that XMRV arose as a lab recombination event in the early 90s is an hypothesis, several studies found it or something like it in the 80s that have been commented on since several times. This hypothesis is accepted far too readily. Even if its correct that recombination created the virus in the lab, pure chance (as I have discussed repeatedly elsewhere) could have created it millions of times in the natural population last century alone. So what if it appeared in a lab culture? They also did not rule out that the virus contaminated the culture. It does that, quite readily as it turns out. If the virus was around, it had a much higher probability of contaminating the culture than a chance recombination event. The recombination event is actually a much more unlikely hypothesis. Please note that I am not saying I know they are wrong, only that we should be sceptical.

The recombination event paper has already been debunked by another under-publicised recombination paper that succeeded it, hasn't it? A paper that Switzer (i think) was involved in showed that there were so many possibilities and opportunities for recombination events to happen, that the theories in first recombination paper were weak... I can't remember all of the details now, without re-reading it all.

I am not saying my model discussed here is correct, only that it fits the facts. I am still completely open to an autoimmune/regulatory problem as the cause, it was where I started in the 90s and it still makes sense. The Rituximab study unfortunately could be either immune or viral, as B cells can be affected by viruses, retroviruses or defects in immune regulation. It could even be due to an unintended side effect of Rituximab, not the B cell depletion at all. This is early days in the research.

If the retrovirus lives in B cells, then that could be one explanation. Didn't JM say that she had created a 'spontaneous' cell line from B cells, suggesting that they are infected and harbour the virus?


I agree with your take on it Alex. There are so many unknown variables with regards to retroviruses that I think the pattern of illness with ME could easily be explained by a retrovirus.

 

[kurt]

Hi Kurt, in 1955 it was shown ME is blood transmissable here in Australia although I have yet to get hold of the paper - I think it involved finding the same lesions in the brain and spine of monkeys some time after infusion. It was quoted several times after that. We also know many patients get sick after blood transfusions - around 5%.

blood transmissability is not exclusive for retroviral infection. For example, we know that ME/CFS patients often harbor active EBV and CMV infections, and those can be transmitted by blood exchange. In fact both those viruses can survive inside a B cell (per the recent study from Norway). Blood banks sometimes screen for CMV, I believe if the blood will be used for infant transfusion or for someone with a weak immune system. So that is a known issue.

A retrovirus can not only cause similar pathology to that found in ME and CFS, it has a slow incubation period. MLLVs are likely to have a much slower incubation period than HIV, and it can take 20 years for someone to get AIDS (not usually perhaps, but its known). Every person could have contracted the retrovirus long before an epidemic, the epidemic was simply a confluence of factors that combined to trigger a retroviral outbreak in people already infected. The incubation period thus matches the coinfection that triggered the retrovirus. The retrovirus could even be passed down generation after generation, awaiting a trigger. Its spread in the population is likely to be a patchwork, not ubiquitous.

Again, this is certainly possible, but also not an exclusive explanation, there are many diseases that take years to develop, including preconditions where disease is activated in epidemic. People who are more immune-compromised will generally become more ill when particularly bad flu strains go around, for example.

The Lipkin study is the final world on XMRV-like MLV association as far as I am concerned. We wont know to a high degree of certainty until then. Even then it does not rule out the existence of an entirely different retrovirus, or even endogenous retrovirus reactivation via some mechanism. Nagalase is often found in patients, and it can come from a retroviral infection, though thats not the only cause. I think there were reports of isolated findings of reverse transcriptase, but I don't think its ever been systematically followed up. If it was followed up and showed very high prevalence of reverse transcriptase in patients, it would clinch it in my view. We know of no other cause for reverse transcriptase.

All good points, although I think there is a fairly high certainty about the MLV family not being present. But there are always things we do not know, could be other viruses or retroviruses involved. But again, we would need a whole model that works, including the transmission vector. If there is a retrovirus that became universal tens of thousands of years ago, then that should not be hard to find, if it can be isolated then it can be sequenced. There are many harmless retroviruses in our environment and I believe even in our bodies that may provide a model for that, but that goes well beyond my knowledge to even discuss. If this type of ancestral retrovirus were an issue in human disease that would seem to be a new angle on retrovirology, maybe that has been discussed already though.

I am not saying my model discussed here is correct, only that it fits the facts. I am still completely open to an autoimmune/regulatory problem as the cause, it was where I started in the 90s and it still makes sense. The Rituximab study unfortunately could be either immune or viral, as B cells can be affected by viruses, retroviruses or defects in immune regulation. It could even be due to an unintended side effect of Rituximab, not the B cell depletion at all. This is early days in the research.

Many models can fit the facts. I don't have a pet theory, I'm an empiricist. The evidence for MLV is weak and getting weaker. The evidence for HGRV is unclear as that is a new speculative theory. I think there are a few theories out there that are promising, such as the GD-MB hypothesis (RichVank), the hyper-sensitivity theories (the Lights and others), and multiple co-infection theories (Garth Nicolson, others). Science will eventually reveal the truth about ME/CFS, although at times I have wondered whether some advancement in medical technology will be required before this disease can be completely unraveled. We seem to have such a complex interaction of symptoms. But then maybe Rich is right after all and who knows, he has a pretty good angle on the new Norwegian study.

To me one of the great questions is: why is there such a high viral tissue load, especially in the gut (but also muscle, including heart muscle)? What causes this? When we know the answer to that, I think we may be close to cracking the origins of ME and CFS. One of my hypotheses, a variant of something I said years ago, about low NK cell function is that it may be deliberate. At some point with a high viral load the body might have started attacking gut or heart, and the immune system was suppressed automatically. in other words, its a survival mechanism. Against this we of course have the issue that some patients with low NK cell cytotoxicity (and lets not forget T cell cytotoxicity is down too) have had the cytotoxicity restored and have not dropped dead, so I am not completely happy with this hypothesis.
The data is looking more and more like there are at least two types of CFS or ME. It is also possible this is subgroups due to genetics or some other factor. I would be interested to know if patients selected from specific outbreaks did not exhibit such subgroups.

Good questions, some type of immune regulation problem, infection in the immune system, or perhaps genetic immune mutation would seem likely. I was told once by an MD who ran a live blood analysis that most ME/CFS patients have a similar cellular profile to Lyme Disease, including cysts living in the WBCs. Something is obviously interfering with our immune response.

I think we will know more when some researcher decides to run a full genomic profile of ME/CFS patients. What are our weak areas? That might help know where to look, what type of opportunistic infection could be taking advantage of our polymorphisms...

For me the great question is why we have so little advocacy, I have never heard of any disease that is scorned the way we are, except maybe Morgellons (I think they are as bad as or even worse off than ME/CFS patients, they are given the label 'delusional parisitosis'). What is it about ME/CFS patients that makes people want to avoid us rather than help us?

 

[RustyJ]

A small but stable percent of post-viral patients go on to develop ME/CFS after EBV, parvo, Lyme, and probably others. I believe this puts ME/CFS in a category of genetic precondition plus air-borne or water-borne trigger pathogens.

If this is a core reason for your non-belief in HGRVs, why have you excluded the possibility of a retrovirus from being an air-borne pathogen?

 

[kurt]

It's not a major secret that many of those posters (not all, and not you) who have joined the anti HGRV side of the debate had a less than sympathetic view of ME and certainly it could be argued that the CDC has perpetuated this view over the decades.

I guess that's the problem with lumping people together. There are many people sympathetic to ME/CFs who do not believe the XMRV/HGRV theory has merit.

By now I don't think there are many on this forum who don't know you are against HGRVsl. I mean how many times, on how many threads is it really necessary for you to tell us that you don't believe in HGRVs? If people who are interested in HGRVs are discussing posts, why is it necessary for you to join the debate when it is only to make a negative comment or to reiterate a point you have made before. I can see how this sort of behavior could make posters wishing to discuss HGRVs a little aggressive.

Your final comment about the finality of HGRVs and ME typifies how some of your posts can polarise members. You appear to know/believe for certain that HGRVs are dead, whereas I disagree. Now what this means is that I don't think they are dead, not that I know for certain ME patients have HGRVs. There is a world of difference. Your argument resonates with the closing statments of those negative studies that trumpeted HGRVs are dead. Surely you can see this distinction.

This is all a matter of perspective. From my viewpoint, the pro-XMRV posts all over the forum are often absolutist, as if 'we know ME/CFS is caused by an HGRV so therefore this topic must relate to that'. Because of the aggressive nature of the pro-XMRV crowd over the past two years, many of the people sympathetic to ME/CFS but holding opposing views of XMRV have left or stopped posting. There is nothing wrong with believing the negative studies were right about XMRV.

 

[kurt]

If this is a core reason for your non-belief in HGRVs, why have you excluded the possibility of a retrovirus from being an air-borne pathogen?

Because what I read about MLVs when I studied this issue there was no evidence of airborne infection. You do not get retroviruses from kissing or airborne or even water contact, at least not the retroviruses I have read about. They require blood contact. That may include open sores, but pretty much precludes human outbreaks from casual contact. At least given the evidence at hand. I'm no expert at this but from what I read (admittedly, a few years ago), there are issues of saliva enzymes that inhibit spread of infection from casual contact, and also there must be a certain viral count in the transfer, which is more likely from direct blood contact than from air-borne.

Not sure the transmission issue is the only core reason for me, I also believe the evidence of the negative studies, many of which used well-defined ME/CFS cohorts, more sensitive testing, and ran tests for the entire MLV family. I know at least one study tested their assay against embedded infection (prostate) and proved it worked, the assays were valid. The CDC even used live XMRV fragments to attempt and trigger the reported antibody response. There is no better antibody stimulation test. When evidence builds up like that, disproving their (negative) finding becomes harder.

 

[barbc56]

RustyJ wrote:

It's not a major secret that many of those posters (not all, and not you) who have joined the anti HGRV side of the debate had a less than sympathetic view of ME and certainly it could be argued that the CDC has perpetuated this view over the decades.

Rusty,think of it another way. Possibly it's not a matter of being pro or anti HGRV, but where the science is at this point in time.

Your wording shows how this can be turned into an us vs. them mind set, when it's not necessarily that. This can lead to more contentious dialogue than a subject merits.

It's how science works. As new data comes in, information/knowledge may change.

 

[SilverbladeTE]

Because what I read about MLVs when I studied this issue there was no evidence of airborne infection. You do not get retroviruses from kissing or airborne or even water contact, at least not the retroviruses I have read about. .

Silverblade's Facts of Life #3:
Assumption is the mother of all f*** ups!

hehe, no offence meant
just that because prior pathogens behaved THIS way, does not mean a new one cannot act ANOTHER way, and folk should always be very wary of such.
If a novel disease has actually existed for a very long time, but gone unnnoticed, the odds of it being unusual are greatly higher.

 

[currer]

I do not think a retraction of Lombardi et al will be possible if Silverman and Singh stand by their findings in prostate and breast cancer.

These are two diseases whose rate is rapidly growing for reasons that are unclear and there is a powerful research lobby behind both diseases, especially as breast cancer can affect women with young families.

I do not think that either Silverman or Singh, if they believe in the validity of their findings, are likely to turn away from them without a battle.

So I will be interested to see how their research proceeds. Silverman is still doing research on "XMRV" and getting it published.

 

[currer]

There are some interesting points in Dr.Mikovits talk from the IiME conference, from May 2011, which I am checking out on the DVD as I get time.

The first is that she mentions, (and this is in May, before the BWG concluded) that they were working very hard with the BWG to get their assays to work but the BWG wanted them to adapt their tests to use EDTA instead of heparin anticoagulant as this was how HIV samples were done.

She said that it reduced the efficiency of their tests to 10% (not by 10%) as it destroyed magnesium, and took the LNCAP calls "right off the back of the flask"



The other was that she said that they had used a 2D gel electrophoresis test which had run the antibodies found in their patient samples out onto a gel, which test revealed the specific antigen binding to an antibody.
http://en.wikipedia.org/wiki/Two-dimensional_gel_electrophoresis

She said this test showed there was an HGRV antigen there, it was not a non-specific cross reactivity.

Of course an antigen-antibody complex cannot be formed by contamination.
It is interesting that she stated that the antigen was able to be characterised as an MLV.

Does anybody know how accurately this test can determine the origin of an antigen?

 

[RustyJ]

Because what I read about MLVs when I studied this issue there was no evidence of airborne infection. You do not get retroviruses from kissing or airborne or even water contact, at least not the retroviruses I have read about. They require blood contact. That may include open sores, but pretty much precludes human outbreaks from casual contact. At least given the evidence at hand. I'm no expert at this but from what I read (admittedly, a few years ago), there are issues of saliva enzymes that inhibit spread of infection from casual contact, and also there must be a certain viral count in the transfer, which is more likely from direct blood contact than from air-borne.

Not sure the transmission issue is the only core reason for me, I also believe the evidence of the negative studies, many of which used well-defined ME/CFS cohorts, more sensitive testing, and ran tests for the entire MLV family. I know at least one study tested their assay against embedded infection (prostate) and proved it worked, the assays were valid. The CDC even used live XMRV fragments to attempt and trigger the reported antibody response. There is no better antibody stimulation test. When evidence builds up like that, disproving their (negative) finding becomes harder.

Kurt, this is something the so-called experts that came onto the site claimed. Rather than repeating dangerous assumptions, or deliberate misinformation (because those who made the claims did so to discredit Mikovits, and you are continuing their efforts) here is a little reading for you. What is most disturbing is that most retovirologists should know XMRV has the potential to be aerosolized.

What is even more disturbing is that some retrovirologists have been using JSRV to create recombinant retroviruses. And we already know they can't stop contamination by XMLVs etc.

There is preliminary evidence that HGRVs can be spread by aerosolization (the spread of fine solid particles or liquid droplets in the air). This is not an new characteristic of retroviruses as Jaagsiekte sheep retrovirus (JSRV), a betaretrovirus which is the causative agent of a contagious lung cancer in sheep called Jaagsiekte, or Ovine Pulmonary Adenocarcinoma (OPA)is also transmitted through aerosol spread.[1][2]

More recently, Morozov et al.[3] reported the presence of JSRV-related sequences in healthy and HIV positive Africans.

Dusty Miller et al.[4] has a patent that demonstrates that JSRV envelope protein (Env) can be used to transduce human and other mammalian cells. Hybrid retrovirus packaging cells have been constructed that express the JSRV Env and retrovirus Gag-Pol proteins, and can produce JSRV-pseudotype vectors at high titers. Using high-titer virus the host range for JSRV has been established, and included sheep, human, monkey, bovine and dog cells, but not murine, rat or hamster cells. Retroviral packaging cell lines comprising the JSRV envelope protein, and receptor binding fragments thereof, are provided which transiently and stably produce high titers of recombinant retrovirus particles which can be used to transfer a heterologous gene to a eukaryotic cell.

1. http://www.vetres-archive.org/file/...38_2/Vet.Res._0928-4249_2007_38_2_ART0004.pdf
2. http://en.wikipedia.org/wiki/Jaagsiekte_sheep_retrovirus
3. http://www.moredun.ac.uk/webfm_send/79
4. http://patents.com/us-20030104357.html

http://www.flimecfsforum.com/wiki/index.php?title=HGRV_-_Transmission

 

[markmc20001]

RustyJ wrote:


Rusty,think of it another way. Possibly it's not a matter of being pro or anti HGRV, but where the science is at this point in time.

Your wording shows how this can be turned into an us vs. them mind set, when it's not necessarily that. This can lead to more contentious dialogue than a subject merits.

It's how science works. As new data comes in, information/knowledge may change.

HA! this hasn't been about science ever since the Lombardi paper was released. It's been more like a public relations and political campaign!

It's more accurate to say it has been a brainwashing exercise for weeks in here to drive the message home "XMRV IS DEAD".


Here is the scientific issue boiled down to a simplified form anybody should be able to understand.

The Lombardi Assays were optimized to find various strains of an HGRV virus. All the negative papers designed new tests optimized to find a VP62 clone.

They were looking for two different things, with different tests!


Let me see if I can make it easier to understand. The Lombardi study found a 5 LB bag of Organic Red Washington apples(HGRV's). Somebody along the way created a GMO Green Grannie Smith apple (a clone called vp62). Then somebody outside the original group(who never found the virus) made the Green Apple the "reference standard".

Now all the negative studies designed their tests to find the newly created Green Granny Smith apple reference standard!

No wonder they can't find the 5lb bag of Organic Washington Red Apples, their tests are optimized to find a single Green Grannie Smith GMO apple!

No studies have bothered to replicate the original Lombardi assays that found the virus. New tests were created to find a "clone" determined to be a "reference standard" by somebody outside the original group who actually found the virus.

Things behaving differently under unique scientific conditions.

http://www.mecfsforums.com/index.php/topic,10008.0.html

 

[dannybex]

No studies have bothered to replicate the original Lombardi assays that found the virus. New tests were created to find a "clone" determined to be a "reference standard" by somebody outside the original group who actually found the virus.

A few questions Mark:

How could others replicate the original Lombardi assays if critical information was left out? (sorry, can't remember the name of the agent used that Mikovits described just a few weeks ago...)

Also, how come Mikovits/Lombardi couldn't find the virus in the BWG study? Weren't they in essence 'replicating' their original work?

I dunno...just asking, trying to understand.

 

[Deatheye]

A few questions Mark:
How could others replicate the original Lombardi assays if critical information was left out? (sorry, can't remember the name of the agent used that Mikovits described just a few weeks ago...)

They can't. But that still doesn't change the fact that they didn't. Seems like they thought that part wasn't critical when they released the study. Also I personally wonder if it really is that critical. That wasn't used on all the samples.
I wonder where actually only the samples positiv that where threated with that agent? I hardly can imagine that they woudn't have noticed that. If also others are positiv, I really don't see why it should have been critical at that point or even now.

A few questions Mark:
Also, how come Mikovits/Lombardi couldn't find the virus in the BWG study? Weren't they in essence 'replicating' their original work?

Seems there is contradicting Information out there. The BWG seems to say everyone could do how they like it. But Judy says that they coudn't do how they like to do it on the Invest in ME DVD and that changes adversly effect theyr test. I assume without sitting personally together with judy and the people that answered the BWG FAQ we can't say whats the truth.

 

[barbc56]

Thanks Eco. You are truly a voice of reason. :>)

 

[slovokia]

I think for some people belief in something becomes part of their identity / worldview. Data that questions that belief is treated as an attack on their ego - prompting an essentially emotionally motivated defense. When people are in emotional defense mode their rational side is not available to be engaged. Most human beings are not constitutionally equipped to engage in science because they subject ideas that they agree with to less critical thinking than ideas that they disagree with - i.e. they fit the data to their hypotheses not the other way around.

Judy Mikovits is the kind of person that inspires faith and support among patients. She expresses concern for patients and states that she is doing everything she can to help us. She maintains a posture of confidence, making bold assertive statements. I have not heard many statements from her admitting to any errors or mistakes on her part. Put together these are the attributes that inspire a following - a following which is emotionally disinclined to consider questions of competence. In addition Judy Mikovits possesses a powerful trump card: she can claim the reason other researchers cannot replicate her findings is because of bias against the disease. She is therefore able to place herself in a role similar to that of patients - a minority fighting a majority which is biased against it and disinclined to treat it fairly.

Folks in the scientific community understand the scientific details and can make competency judgments without this baggage. I don't see the opinions of these worlds converging. More likely the controversy will fade away due to other causes.