Comparing PreXMRV-2 gag sequence diversity in laboratory and wild mice

[barbc56]

About 10-15% of CFS/ME cases commence following a vaccination. But this can never be discussed either.
I was present at a talk at the London School of Hygeine and Tropical Medicine when this question was asked - and none of the doctors on the panel would respond. In fact they behaved as if they did not hear the question.

Where did you get this information? I'm just speculating here but maybe the researchers have been a bit weary about these question as vaccinations have not been linked with human illness except for very rare occasions. There are many studies that show this. There are lots of us who did not get this DD after vaccinations.

Antecdotal reports about illness after a vaccination are not always reliable as people tend to think of the last event that comes to their mind as a causative factor and a vaccination comes to mind when the likelyhood is probably coincidence.

Barb C.:>)

 

[free at last]

Hi Jace, it is a virus that becomes part of the human system like a retrovirus. like chicken pox ect.one that can not be eliminated intirely.one that can go dormant. Hence recovery.

The immune system can have trouble in keeping the virus in check. Either because of a weakened immune system, or the virus being lifelong becoming a pest that the immune system can struggle with.

But dont underestimate, what very healthy food and possibly supplements can do. to strengthen the immune system into getting the upper hand.It can become a visiouse circle with people who have this illness. Lack of sleep also making the problem worse for many. With out good consistent sleep. the immune system can fail to fight the virus. as the immune system just gets weaker and weaker. The way to combat this. is to find a way to get the sleep needed. rest rest and more rest. sleep sleep and more sleep. I do belive feeding the body with high nutient vegetable and protein foods can help tip the balance in favour of the immune system ( i think it did with me ) something did ? a combination of going from terrible sleep. poor diet. to good consistent sleep and nutient explosions from many many different types of vegetables. If you look at each veg and what it contains. and what it can do for the human body. you will find many many things that are miracle substances. like the red pigment in tomatoes for example showing protection agaisnt heart disease. as a example. many foods and substances have yet to be fully understood in there protection abillitys. So the best bet. is to feed the body as many diffent types of these foods as one can find. buy. or tolerate. as a example kail deep red peppers. beetroot. spinnach onion ( different types spring. red white ect. garlic ( raw ) raddish. celery. lettuce carrot avocado. on and on you get the picture. oily fish for protien and oils. fruit for vit c. These ideas will not cure fatal illness like aids. but viruses that can be beaten. or at least controlled. as i know this one can. you are in affect fighting back with a much stronger army. than if you do not live like this. It took years of living like this to get this under control. but it happened thats the important point. i took some suppliments too. but im unsure how or if they helped. they may. they may not have ?

 

[currer]

When I was studying I was taught that new diseases moving into a group (such as the young) were a public health alert. Because the young are the healthiest group in the population and ought not to become ill. So if young people are getting ill this must be investigated.

Yet all the efforts on our disease hitherto have been devoted to sweeping the problem under the carpet. This is utterly irresponsible.

 

[currer]

"Where did you get this information?"

British ME Association. Dr Charles Shepherd took a particular interest in ME cases following hepatitis B vaccination.
He stated that this vaccination can lead to a particularly nasty form of ME.

"Living with ME" Dr Charles Shepherd pages 35-37

But I am forced to admit - the percentage in the book is 5% following vaccination. I remember it higher, but cannot find a reference now.

 

[Bob]

Where did you get this information? Could the researchers have been a bit stunned by the question as vaccinations have not been linked with human illness except for very rare occasions? There are many studies that show this. I'm sure there are lots of us who did not get this DD after vaccinations.

Antecdotal reports about illness after a vaccination are not always reliable as people tend to think of the last event that comes to their mind as a causative factor and a vaccination comes to mind when the likelyhood is probably coincidence.

Barb C.:>)

I don't know if there has been any research into this, beyond anecdotal reports and the collecting of information by general practitioners, but vaccinations have long been thought to be associated with ME, especially Hep B vaccines.

 

[free at last]

As you probably know, Jace, I've always rigorously defended XMRV research. And I have often agreed with what you've said above, especially as many people have often appeared to be prematurely very motivated to discredit all research into XMRV, especially in relation to ME. But this thread has been very civilised, with people only expressing honest opinions, based on their understanding of the science.

I've got to the point now where I find it very difficult to believe that there are any retroviruses involved in ME. It's been at least two years now since the Lombardi paper, and there haven't been any convincing positive retroviral studies into ME. But there must have been loads of scientists attempting to replicate the research, or trying to find XMRV-related viruses, but unable to. Negative studies often don't get published, and just get abandoned.

Also, Judy has mentioned contamination on a number of occasions now. The latest media article is just one of those occasions. Obviously, contamination is an issue, and could explain many of the positive results. I know it doesn't explain everything, but neither have there been any other convincing explanations for the various positive MLV results that have been backed up by research results.

I'm still fascinated by retroviral research, and I'm looking forward to watching it continue. I think retroviruses could play a role in other diseases, such as breast cancer. But with ME, I'm not convinced, and I'm looking elsewhere for research developments now, such as Rituximab, and the ongoing biomarker research, and Lipkin's CFI pathogen study which I hope could be ground-breaking.

Also, we've been promised specific results of next generation sequencing from the WPI, and from Dr Snyderman, for months now, or years, and the results have not come to light. So I can only draw one conclusion from that, and that's that they did not confirm their expectations.

So, it appears that: next generation sequencing has not confirmed the other research results; there has been contamination; there have been no confirmation studies for a human virus in ME; and Judy has not released any further information regarding her other retroviruses in two years, but has now discussed contamination issues in public.

If anyone wants to remind me if I'm missing anything that would convince me here, then I'm open minded, and receptive.

I also think it's important to remember that retrovirologists around the world will have been attempting to replicate XMRV research and research into related MLVs, such as with the recent PreXMRV-2 paper. Research into MLVs has probably accelerated since the discovery of XMRV, with loads of resources available. There are going to be many scientists who are interested in finding out more about the contamination of cell lines, and the various MLVs that are so ubiquitous.

I agree Bob. xrmrv appears dead in the water. But there is a virus of somekind at the heart of this. there was for me. and there appears to be for many others. with flu type onset

 

[Bob]

I agree Bob. xrmrv appears dead in the water. But there is a virus of somekind at the heart of this. there was for me. and there appears to be for many others. with flu type onset

That's why Lipkin's CFI pathogen study will be so interesting. If he finds any pathogens then they will be definite active viruses, present in our bodies causing problems. If he finds Herpes viruses, for example, it won't be like other past studies in which vague antibody results are relied upon, but if he finds something then it will be a definite active virus, causing problems. And the results will be compared to healthy controls. If there are any retroviruses present, then these should show up, in theory, as well. I think it's very hopeful, especially with all the other research being planned or carried out at the moment. Lerner has had some good results using antivirals with ME patients who test positive for Herpes antibodies, so it will interesting to compare Lipkin's results with that sort of research. But completely new and unexpected viruses could potentially show up, including any enteroviruses for example, which have long been associated with ME.

 

[Marco]

I wonder would Dr Miller be so kind as to comment on the following musings?

Stepping back a little from the details of this specific virus or viruses any association of a pathogen with ME/CFS or any other disease has to be plausible in the context of the natural history of the illness. Clearly if a virus or retrovirus contributes to ME/CFS then it rarely results in an acute infection which is highly pathogenic.

In evolutionary terms a successful organism is one that is optimally adapted to its host environment and which is able to ensure the continuation of its 'pattern' via reproduction.

In viral terms it must survive the response of the host immune system and replicate. However in the absence of transmission to another host its lifespan is limited to that of the original host. If we assume that transmission is largely restricted to horizontal transmission via sex or vertical transmission via the mother's milk then the host mammal must reach sexual maturity before transmission to another host can occur. An outbreak of a highly pathogenic virus resulting in high mortality rates relying on transmission via these methods would be more likely to 'burn out' relatively quickly, particularly in isolated populations, and therefore in evolutionary terms would not be considered well adapted or successful.

From this perspective I would be interested to know :

how you would characterise a well adapted viral pathogen?

given that, again in evolutionary terms, well adapted viruses are more likely to proliferate, would it logically follow that the majority of successful viruses are more likely to result in chronic, low-mortality infections and that highly pathogenic viruses represent the tip of the iceberg? Albeit that our modern population patterns may favour the survival of these less adapted pathogens?

If this is the case, given that the disease burden attributable to chronic illnesses (many of which are of unknown aetiology and some of which have a suspected viral/retroviral or HERV association) is likely to far outweigh the admittedly tragic burden attributable to highly pathogenic viruses, could it be argued that focusing mainly on those viruses that result in clear pathology following acute infection is a misplaced skewing of resources?

IF a pathogen is involved in ME/CFS should we be looking for something that doesn't appear acutely pathogenic?

 

[jace]

Something's going on with the immune system too, I've not had so much as a cold in the three and a half years that I've been ill, despite being around snotty grandkids, who stick mucus-laden fingers up my nose.

I've always eaten a majority of fresh veg and fruit, quality protein etc. Never did like junk food.

I am not ready to say that the retroviral involvement in ME is proven false. I am not ready to say that it is proven true. I am awaiting further evidence, and am very aware of the way information can be skewed.

 

[Ecoclimber]

If you take into consideration the various historical outbreaks throughout the years in London, L.A. Hospital, Lyndonville, Lake Tahoe and elsewhere, the etiology of this illness demonstrated at times a spontaneous outburst via aerosol transmission with a short incubation periods of 4-5 days. You also have the etiology of a significant number of patients failing to recover after a post viral infection. One will have to consider this atypical behavior for a retrovirus.

Epidemiological investigation into this illness would be helpful. Considering that the Bubonic plague is a zoonotic disease caused by bacteria spread by fleas on rodents, it is too early in the game, in my opinion to be determinant the causative nature of this illness whether viral, bacterial, fungal, retroviral or a combination of one or more of the these, plus a genetic predisposition whether through natural or causal toxin exposure.

Eco

 

[FancyMyBlood]

Let me first be clear that I do not believe XMRV is a human pathogen and/or is associated with any disease.

Nonetheless, I was just reading an article in a Dutch science magazine and it was about the AIDS patient Timothy Brown.

In 2009 a Berlin research team reported in NEJM that they couldn't detect HIV after 20 months Brown recieved two stem cell therapies to treat leukemia. They found a donor who had a genetic mutation that makes them unsensitive to HIV and hoped it would eradicate HIV in Brown's body. In that 2009 NEJM paper they were quite careful and used the words 'long-term control of HIV'.
In 2011 they still couldn't detect HIV and published a paper in Blood 'evidence for the cure of HIV'. Now it gets interesting, because in june 2012 another researcher (Steven Yukl) claimed to have found minute traces of HIV in Brown's blood. Some other could also detect it, while others couldn't detect any trace of HIV (sounds familiar?). The story continues with some other strange plots (not really interesting for us ME/CFS patients), but it raises some issues about sensitivity of detection and when/if we can be sure there is no virus present in the human body.

I don't think this has any relevance for XMRV research. Mainly because Mikovits was unable to replicate here own findings and although some conspiracy theorists will never admit XMRV/HGRV is not present, the science is settled
.
However, it does make me wonder if this story might have any relevance for ME/CFS related viral research. As we all know there are papers of HHV-6/enterovirus/parvovirus infection/reactivation while others can't find anything.....

Maybe Dusty Miller can shed some light on this matter?

 

[Dusty Miller]

Dr. Miller, you posted yourself the quote from Genbank that says

pu·ta·tive (py

t

-t

v)​

adj.​

Generally regarded as such; supposed. See Synonyms at supposed.​

​

[Middle English, from Old French putatif, from Late Latin put

t

vus, from Latin put

re, to prune, think; see pau-2 in Indo-European roots.]
You have also posted what is the sequence for a protein, extrapolated from the protein linking it to the env of 'XMRV' more specifically VP62. If they had the env sequence, surely they would have posted the env sequence? Without that, there is no way we can be sure that this is VP62.

Of course I know what putative means. I like the term 'predicted' instead, but no matter.

What you need to know is that molecular biologists discovered some time ago that machinery exists in every cell to convert DNA information to RNA, and then to specific proteins. The code for this translation is well understood based on countless experiments. So having the DNA of an organism, such as the VP62 or 22Rv1 virus, or even your genome Jace, allows one to predict the sequences of the proteins made by that organism. Because the mechanism of conversion of DNA to protein is so well understood, most scientists no longer sequence the proteins made by a gene. However, protein sequencing is still done to resolve subtle issues, such as post-translational modifications that can occur to proteins. But, to be perfectly honest, the predicted protein sequences are called 'putative' or 'predicted' because the proteins often have not actually been sequenced.

There was a comment earlier in one of these forums implying that the Env PROTEIN of one of the XMRV viruses had been sequenced, and the DNA sequence of the virus was inferred from the protein sequence. This of course cannot be done accurately because of the degeneracy of the triplet code for individual amino acids. And, this was not done for any of the XMRV isolates. Scientists routinely clone DNA directly, or clone DNA copied from RNA, to infer the sequences of the proteins made by the organism, which is much easier than sequencing the proteins. This was what was done for all of the XMRV and related virus isolates that we have been discussing.

Anyway, if you still don't understand what I am saying, I think it's time for you to do some reading of one or more of the basic molecular biology and/or virology textbooks to get a better appreciation for what is going on here.

 

[VillageLife]

Hi Dr Miller,

Dr Ruscetti has said he believes its a family of Gammaretroviruses, I think because of his experience and skills, people must listen to him and carry on researching this.

 

[Mula]

I can't imagine why you persist in calling the 22Rv1/CWR-R1 sequence (http://www.ncbi.nlm.nih.gov/nuccore/FN692043.2) incomplete. I just did a BLAST search on this sequence, and it matches the VP62 XMRV sequence very well, with only 5 base mismatches and two single-base gaps. We know the VP62 sequence is complete because several groups, including my own, have been able to generate infectious virus from the plasmid containing the VP62 XMRV sequence. Therefore, the 22Rv1/CWR-R1 sequence also appears to be complete. The two single-base gaps in the sequence comparison are downstream of the Env coding region in both viruses, so they don't affect the protein coding regions. Both env genes encode proteins of 645 amino acids, with only one difference between the VP62 and 22Rv1/CWR-R1 Env amino acid sequences (top sequence = VP62, middle sequence = shared amino acids, bottom = 22Rv1/CWR-R1 sequence):

...Query 1 MESPAFSKPLKDKINPWGPLIIMGILVRAGASVQRDSPHQVFNVTWKITNLMTGQTANAT 60
...........MESPAFSKPLKDKINPWGPLIIMGILVRAGASVQRDSPHQVFNVTWKITNLMTGQTANAT
Sbjct 5754 MESPAFSKPLKDKINPWGPLIIMGILVRAGASVQRDSPHQVFNVTWKITNLMTGQTANAT 5933

..Query 61 SLLGTMTDTFPKLYFDLCDLVGDNWDDPEPDIGDGCRSPGGRKRTRLYDFYVCPGHTVLT 120
...........SLLGTMTDTFPKLYFDLCDLVGDNWDDPEPDIGDGCRSPGGRKRTRLYDFYVCPGHTVLT
Sbjct 5934 SLLGTMTDTFPKLYFDLCDLVGDNWDDPEPDIGDGCRSPGGRKRTRLYDFYVCPGHTVLT 6113

.Query 121 GCGGPREGYCGKWGCETTGQAYWKPSSSWDLISLKRGNTPKGQGPCFDSSVGSGSIQGAT 180
...........GCGGPREGYCGKWGCETTGQAYWKPSSSWDLISLKRGNTPKGQGPCFDSSVGSGSIQGAT
Sbjct 6114 GCGGPREGYCGKWGCETTGQAYWKPSSSWDLISLKRGNTPKGQGPCFDSSVGSGSIQGAT 6293

.Query 181 PGGRCNPLVLEFTDAGKRASWDAPKTWGLRLYRSTGADPVTLFSLTRQVLNVGPRVPIGP 240
...........PGGRCNPLVLEFTDAGKRASWDAPKTWGLRLYRSTGADPVTLFSLTRQVLNVGPRVPIGP
Sbjct 6294 PGGRCNPLVLEFTDAGKRASWDAPKTWGLRLYRSTGADPVTLFSLTRQVLNVGPRVPIGP 6473

.Query 241 NPVITEQLPPSQPVQIMLPRPPRPPPSGAASMVPGAPPPSQQPGTGDRLLNLVEGAYQAL 300
...........NPVITEQLPPSQPVQIMLPRPPRPPPSGAASMVPGAPPPSQQPGTGDRLLNLVEGAYQAL
Sbjct 6474 NPVITEQLPPSQPVQIMLPRPPRPPPSGAASMVPGAPPPSQQPGTGDRLLNLVEGAYQAL 6653

.Query 301 NLTSPDKTQECWLCLVSGPPYYEGVAVLGTYSNHTSAPANCSVTSQHKLTLSEVTGQGLC 360
...........NLTSPDKTQECWLCLVSGPPYYEGVAVLGTYSNHTSAPANCSVTSQHKLTLSEVTGQGLC
Sbjct 6654 NLTSPDKTQECWLCLVSGPPYYEGVAVLGTYSNHTSAPANCSVTSQHKLTLSEVTGQGLC 6833

.Query 361 IGAVPKTHQALCNTTQKTSDGSYYLASPAGTIWACSTGLTPCLSTTVLNLTTDYCVLVEL 420
...........IGAVPKTHQALCNTTQKTSDGSYYLASPAGTIWACSTGLTPCLSTTVLNLTTDYCVLVEL
Sbjct 6834 IGAVPKTHQALCNTTQKTSDGSYYLASPAGTIWACSTGLTPCLSTTVLNLTTDYCVLVEL 7013

.Query 421 WPKVTYHSPNYVYGQFEKKTKYKREPVSLTLALLLGGLTMGGIAAGVGTGTTALVATKQF 480
...........WPKVTYHSPNYVYGQFEKKTKYKREPVSLTLALLLGGLTMGGIAAGVGTGTTALVATKQF
Sbjct 7014 WPKVTYHSPNYVYGQFEKKTKYKREPVSLTLALLLGGLTMGGIAAGVGTGTTALVATKQF 7193

.Query 481 EQLQAAIHTDLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFY 540
...........EQLQAAIHTDLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFY
Sbjct 7194 EQLQAAIHTDLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFY 7373

.Query 541 ADHTGVVRDSMAKLRERLNQRQKLFESRQGWFEGLFNRSPWFTTLISTIMGPLIVLLLIL 600
...........ADHTGVVRDSMAKLRERLNQRQKLFES QGWFEGLFNRSPWFTTLISTIMGPLIVLLLIL
Sbjct 7374 ADHTGVVRDSMAKLRERLNQRQKLFESGQGWFEGLFNRSPWFTTLISTIMGPLIVLLLIL 7553

.Query 601 LFGPCILNRLVQFVKDRISVVQALVLTQQYHQLKSIDPEEVESRE 645
...........LFGPCILNRLVQFVKDRISVVQALVLTQQYHQLKSIDPEEVESRE
Sbjct 7554 LFGPCILNRLVQFVKDRISVVQALVLTQQYHQLKSIDPEEVESRE 7688

As I stated earlier in this thread, the fact that the env gene is not annotated in the 22Rv1/CWR-R1 sequence doesn't mean that it is not there. Analysis of the GenBank sequence shows clearly that it is present.

Regarding your question of why separate sequences for the 22Rv1 and CWR-R1 viruses are not provided, I believe the authors of the study found that the CWR-R1 sequence matched that of the 22Rv1 sequence exactly, and because the two viruses represent descendants of the same original recombinant virus, they decided to report only one sequence. Why report two sequences when they are identical and derive from the same parental virus?

If you are still confused, please tell me exactly what bothers you.

There is no envelop gene for this sequence and it is fully annotated as a being "putative" which is a proposed sequence. Without this data a confirmation study is not possible.

/product="putative envelope polyprotein"

To compare two viruses from separate cell lines an individual virus is necessary from each, not as we have here which is an incomplete sequence derived from both cell lines.

 

[currer]

What concerns me is the disingenuousness of repeatedly conflating the XMRV sequence with PMRVs. Why are we repeatedly subjected to these arguments?

We all know that "XMRV" is not what Dr Mikovits thought she found - when I met her at the Invest in ME conference last year she had found a range of polytropic retroviruses.
The XMRV section of the original Science paper was retracted with her agreement.
Why are we continually bombarded with repeated "proofs" of the non-existence of XMRV?

If there are retroviral fragments that have passed into the human population and are capable of causing disease either directly by infecting immune cells, or indirectly by reactivating endogenous HERVs or just by sitting around and provoking an autoimmune reaction - it aint going to be XMRV - but it could be one of those adventitious agents JT1024 posted about earlier that the FDA and Dr Stoye are concerned about.
Risks Associated with Retroelements: Lessons from Mammalian SystemsJonathan Stoye, PhD, Head of the Division of Virology, MRC National Institute for Medical Research

The public narrative is that "XMRV" is all over. But behind the scenes there is ample evidence that the very concerns "XMRV" raised are still very much in the minds of its' most vocal opponents.

 

[Mula]

"Where did you get this information?"

British ME Association. Dr Charles Shepherd took a particular interest in ME cases following hepatitis B vaccination.
He stated that this vaccination can lead to a particularly nasty form of ME.

"Living with ME" Dr Charles Shepherd pages 35-37

But I am forced to admit - the percentage in the book is 5% following vaccination. I remember it higher, but cannot find a reference now.

There was some data in these articles. Immune changes are able to activate MLVs which is how I have been convinced this is a trigger for a latent infection.
http://www.cfids.org/archives/2001rr/2001-rr1-article03.asp
http://www.investinme.org/InfoCentre-vaccines-popup-1.htm

approximately 60% of CFS patients experience some form of exacerbation in their fatigue and flulike symptoms (sometimes quite marked) following an influenza vaccine

 

[Dusty Miller]

An initial opinion was all I asked for.
BTW: I'm sure your cats return that look. I often wonder where cats get their secret information.

I did have a comment on the example of the "harmless" ERV in NZB mice. Those mice were carefully selected for health. Other lines formed from the same basic NZ genetic stock are used as laboratory models of a number of diseases, including chronic lymphocytic leukemia, lupus, other autoimmune disorders and neurodevelopmental pathology. Even a lesser degree of selection would allow me to argue that polio virus is harmless to properly-selected humans.

I agree with your concern about my example of the "harmless" xenotropic ERV in NZB mice. I read over some of the early descriptions of the generation of inbred mice in New Zealand, and some of Jay Levy's publications from the 1970's on the detection of xenotropic virus in these and other strains of mice. While there appears to be no proof that the NZB xenotropic retrovirus causes disease in these mice, a role of the virus in these diseases cannot be ruled out either. The other possible source of some of the disease phenotypes in these mice is the inbreeding process, which can result in fixation of disease causing mutations. It is interesting that Levy detected production of xenotropic retrovirus(es) in NIH Swiss and C57 Bl/6 mice, two inbred mouse strains that appear to be relatively healthy.

 

[currer]

There was some data in these articles. Immune changes are able to activate MLVs which is how I have been convinced this is a trigger for a latent infection.
http://www.cfids.org/archives/2001rr/2001-rr1-article03.asp
http://www.investinme.org/InfoCentre-vaccines-popup-1.htm

Thanks for finding this for me Mula.
I used to work for a large ME support group and over the years noticed that Hep B was quite a commonly mentioned trigger for this illness.

Dr Shepherd has always been open about his concerns regarding this connection. Now I wonder (since becoming so much more cynical) if his openness could have contributed to some of the difficulties we have in getting research done.
Could ME have been quietly "blacklisted" and research deflected into "harmless fields because of this?

http://www.cfids.org/archives/2001rr/2001-rr1-article03.asp
"Hepatitis vaccines are highly immunogenic compounds, and a number of possible explanations exist as to why they may be more likely to trigger CFS.

One explanation involves a preexisting genetic susceptibility, which after antigenic stimulation with HBV, results in a pathological process (possibly involving immune complex formation) leading to a clinical disease.

Another explanation is that a hypersensitivity reaction occurs to a component of HBV, such as the preservative thimerosal.6

Researchers in Canada, who made similar observations of a link between HBV and CFS, hypothesized that this may involve an autoimmune reaction with a microscopic form of demyelination not visible on magnetic resonance imaging.7

Despite growing anecdotal evidence from other experienced physicians who also believe that HBV can precipitate CFS,2 vaccine manufacturers do not acknowledge any causal link. In fact, a report by an independent working group in Canada that dismissed any such causal link is frequently quoted as a reason for dismissing these claims, even though it contained some very questionable assumptions to support the conclusions.8"

 

[currer]

http://www.investinme.org/InfoCentre-vaccines-popup-1.htm
"By late 1994 Dr Shepherd became so concerned about a steady influx of notifications on cases of hepatitis B vaccines precipitating an ME-like illness, that he submitted a short report to The Lancet. Alas the journal declined to publish his observations"
(So this was reported eighteen years ago.)

http://www.cfids.org/archives/2001rr/2001-rr1-article03.asp
Not surprisingly, patients with possible vaccine-induced CFS often face considerable difficulty in obtaining disability benefits on the grounds of permanent ill health. However, some of my patients in the U.K. have successfully argued their cases and been awarded injury payments on the grounds that HBV given for occupational health reasons caused their CFS. I am also involved in a number of cases where the debate is likely to be settled in court.

So I think we can assume that the pharmaceutical companies are aware of the link between their products and ME

 

[Wally]

I agree with your concern about my example of the "harmless" xenotropic ERV in NZB mice. I read over some of the early descriptions of the generation of inbred mice in New Zealand, and some of Jay Levy's publications from the 1970's on the detection of xenotropic virus in these and other strains of mice. While there appears to be no proof that the NZB xenotropic retrovirus causes disease in these mice, a role of the virus in these diseases cannot be ruled out either. The other possible source of some of the disease phenotypes in these mice is the inbreeding process, which can result in fixation of disease causing mutations. It is interesting that Levy detected production of xenotropic retrovirus(es) in NIH Swiss and C57 Bl/6 mice, two inbred mouse strains that appear to be relatively healthy.

I agree with your concern about my example of the "harmless" xenotropic ERV in NZB mice. I read over some of the early descriptions of the generation of inbred mice in New Zealand, and some of Jay Levy's publications from the 1970's on the detection of xenotropic virus in these and other strains of mice. While there appears to be no proof that the NZB xenotropic retrovirus causes disease in these mice, a role of the virus in these diseases cannot be ruled out either. The other possible source of some of the disease phenotypes in these mice is the inbreeding process, which can result in fixation of disease causing mutations. It is interesting that Levy detected production of xenotropic retrovirus(es) in NIH Swiss and C57 Bl/6 mice, two inbred mouse strains that appear to be relatively healthy.

I do not have a science background nor do I have the best cognitive function due to problems that arise from the illness that I am suffering from. However, in my past life I was a lawyer and I have been watching and reading much of the debate go back and forth about XMRV and retroviruses. From my non-scientific background, but with some analytical capacity left in my brain, I would like to ask a question that I can't seem to find directly addressed and continues to me to feel like the elephant in the room. So here goes my attempt to ask a question that will help me to understand where the divergent views on this subject stand.

1) Has retroviral involvement in the disease process known as ME, CFS and/or MECFS been scientifically proven to not exist in these particular illnesses?

2) If yes, can someone explain in layman terms exactly how the determination has been made that there is no retroviral involvement in these illnesses?

If I need to be more specific with my question regarding "retroviral involvement", I will be glad to clarify how I am using this term.

Thanks. Wally.