Six strains of XMRV so far!

gracenote

All shall be well . . .
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The paper asks a lot of very interesting questions which future research will need to answer, hopefully soon.

Pandoras Box?

The proposed pathobiology of XMRV-related viruses in mice and other species opens a Pandoras box of medical issues.

Does XMRV induce a primary immunodeficiency?

Are lymphocytes the primary target cells in the periphery, with microglial or other support cells playing that role in the central nervous system?

Is XMRV neurotropic and capable of inducing the cognitive, autonomic, and nociceptive changes typical of CFS? Are there readily detectable plasma or cerebrospinal fluid biomarkers of XMRV infection, activation, and transmissibility?

How is XMRV spread?

Do the current data implicate transmission by plasma, leukocytes, gammaglobulin, or other blood products?

Are there indications of fatiguing illnesses in clusters of previously healthy individuals who have received blood transfusions?

Is XMRV transmitted sexually or via saliva?

Evidence of infection in 3.7% of the healthy population was presented. Are these individuals at risk for CFS, fibromyalgia, related syndromes, or even leukemia or prostate cancer?

Does XMRV play a role in the CFS that follows immunocompromise by chemotherapy for cancer or lupus?
 
K

_Kim_

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Another interesting 'tidbit':

It is not known when XMRV began to infect humans, but it may have been within the last few hundreds of generations given the 99% identity between the six genomes that have been sequenced to date from activated CFS leukocytes and advanced prostate cancers
[2, 3, 14]. These differ by only about 30 of 8000 nucleotides, with many of the replacements occurring in nontranslated regions of the virus, or as silent polymorphisms in the third position of codons that do not change protein sequences. Xenotropic infection may have occurred during a period in which mice were a morsel in the human diet.

 
K

_Kim_

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Here's a cautionary warning regarding antiretroviral treatment:

Drugs directed at preventing docking of XMRV to XPR-1 are also conceivable. However, before thoughtfully planned antiviral drug therapy clinical trials are started in patients with CFS and, potentially, prostate cancer, we must consider the potential risk of developing drug-resistant XMRV if single antiviral agents are used.
 

gracenote

All shall be well . . .
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I don't mind this skepticism at all. This paper takes CFS seriously and is looking at real studies. Ain't it grand?

The new finding of XMRV in CFS must make us pause and take a fresh look at these frustrated and disillusioned victims of medical neglect. At the same time, we must maintain skepticism about this viral etiology given the history of other inferred causative agents, such as Epstein-Barr virus; entero- virus; cytomegalovirus; neurotropic herpes types 6 and 8; mycoplasma; Q fever; Murray Valley encephalitis; other microbes; specific genotypes; and an array of immune deficits ranging from low CD4, CD8, and natural killer cell activities to various antinuclear antibodies to cytokine imbalances [68].

6. Kerr JR, Burke B, Petty R, et al.: Seven genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis: a detailed
analysis of gene networks and clinical phenotypes. J Clin Pathol 2008, 61:730739.

7. Lorusso L, Mikhaylova SV, Capelli E, et al.: Immunological aspects of chronic fatigue syndrome. Autoimmun Rev 2009, 8:287291.

8. Fletcher MA, Zeng XR, Barnes Z, et al.: Plasma cytokines in women with chronic fatigue syndrome. J Transl Med 2009, 7:96.
Another author comment.

14. Coffin JM, Stoye JP: Virology. A new virus for old diseases? Science 2009, 326:530531. Coffin brings his 40 years of experience with retroviruses to this informative editorial that introduces the findings of Lombardi et al. [2].
 

hvs

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I don't mind this skepticism at all. This paper takes CFS seriously and is looking at real studies. Ain't it grand?
Right, the vast majority of us on this board don't mind informed skepticism offered in professional, good faith. Indeed, we seek it out so that we can be better informed.
We object to the corrupt and unprofessional (Wessley et al) and those who offer skepticism because they're being patronizing (they know better than us) or acting based on emotion (they're somehow threatened by the outcome).
This is good stuff.
 

Dr. Yes

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At the same time, we must maintain skepticism about this viral etiology given the history of other inferred causative agents, such as Epstein-Barr virus; entero- virus; cytomegalovirus; neurotropic herpes types 6 and 8; mycoplasma; Q fever; Murray Valley encephalitis; other microbes; specific genotypes; and an array of immune deficits ranging from low CD4, CD8, and natural killer cell activities to various antinuclear antibodies to cytokine imbalances [6–8].
I agree Gracenote; I don't mind that comment in context (but I would say that 'objectivity' is the word he should have used... most doctors I run into are over-skeptical about CFS to the point of losing objectivity). What really bugs me about that passage is that he knocks a bunch of pathogens that are still being investigated as potentially causative! I also don't know why he considers findings on low natural killer cell activity insignificant or as some sort of red herring; the WPI certainly doesn't. Comments like that will make it more difficult for us if XMRV turns out NOT to be a causative agent; they just add to the pile of rubbish that buries other significant findings in ME/CFS research.
 

hvs

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What really bugs me about that passage is that he knocks a bunch of pathogens that are still being investigated as potentially causative! I also don't know why he considers findings on low natural killer cell activity insignificant or as some sort of red herring; the WPI certainly doesn't. Comments like that will make it more difficult for us if XMRV turns out NOT to be a causative agent; they just add to the pile of rubbish that buries other significant findings in ME/CFS research.
Great point, Dr. Yes. It's not like we've ever had the money to do big studies of EBV, HHV6, genes, NK cells, RNaseL, PEM, etc. etc. We haven't had the basic shoeleather epidemiology that other diseases have. Unbelievable how much goes back to that central traumatic event in this narrative--CDC trainee Gary Holmes' junket to Tahoe followed by the capture of CFS by James Jones and Emory.
 

bullybeef

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When I first heard XMRV originated from mice, my first thought in regards to the media was: The New Plague (yeah, I know it was rats, but you catch my drift). It makes sense there could be many more people infected, than there are with other viruses. Mice are everywhere, particularly in the western world, and there always pretty close to us.

I hate those mieces to pieces!!!

The biggest scandal out of all of this, is if someone had a suspicion that a retrovirus as been secretly infecting humans for generations, and the powers did nothing. Funnily enough, we know this has happened.
 

serenity

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poor little mices, they are fellow sufferers. hate the disease, but the poor little critters don't want it or deserve it or mean to pass it on any more than we do.
poor pookies
 
R

Robin

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When I first heard XMRV originated from mice, my first thought in regards to the media was: The New Plague (yeah, I know it was rats, but you catch my drift). It makes sense there could be many more people infected, than there are with other viruses. Mice are everywhere, particularly in the western world, and there always pretty close to us.

I hate those mieces to pieces!!!

The biggest scandal out of all of this, is if someone had a suspicion that a retrovirus as been secretly infecting humans for generations, and the powers did nothing. Funnily enough, we know this has happened.
Probably what happened is that there was a jump from mice to people at some point the virus adapted to live in a human host. If XMRV like HIV it is not carried by an animal host like plague or hantavirus; you have to get it from a person. So, while the mieces are likely to blame for the progenitor virus, you can rest assured that it probably gave them leukemia. :)

I have some questions for the smarties: XMRV is a slow replicator/low mutator, as Coffin said at CFSAC. Goff speculated that replication may not even be happening. Unlike HIV the strains are rather homogenous. This has been brought up as a criticism of the XMRV --> ME/CFS hypothesis (on certain science blogs that shall remain unnamed!)

So, what are the implications for treatment? AIDS drugs work by stopping replication. If XMRV doesn't replicate much, how can it be treated? I know this has been discussed before but I can't remember much about it, nor can I find the discussion.

Anyone want to give it a stab?
 
C

Cloud

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Here's a cautionary warning regarding antiretroviral treatment:
"Drugs directed at preventing docking of XMRV to XPR-1 are also conceivable. However, before thoughtfully planned antiviral drug therapy clinical trials are started in patients with CFS and, potentially, prostate cancer, we must consider the potential risk of developing drug-resistant XMRV if single antiviral agents are used".


Indeed the main reason I would not throw anti retrovirals (especially just one) at xmrv at this point.
 

FernRhizome

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I am posting this for another member who didn't want to post themselves and who pointed out the following:

I think the 'six strains' of XMRV mentioned are miscontextualized. As the quote from the paper explains, the author was talking about the six different XMRV isolates which have been fully sequenced which have shown 99% identity, which isn't really the same as there being six different strains of XMRV.

Does anyone know how to change the title of this thread? Should it be retitled Six Isolates rather than Six Strains? ~Fern
 

Dr. Yes

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I think the 'six strains' of XMRV mentioned are miscontextualized. As the quote from the paper explains, the author was talking about the six different XMRV isolates which have been fully sequenced which have shown 99% identity, which isn't really the same as there being six different strains of XMRV.
Actually, the word "strains" is also used in the Science article, even in reference to two isolates that differ by only 6 nucleotides each from the prostate cancer strain VP62. (They call these "CFS XMRV strains 1106 and 1178".)
 
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I don't know if my mind is just not working, but this seems like a lot of talk and thin on answers. So is it right that the only new info in this study is six strains (or whatever word you want to use)?

Otherwise, seems like he just raises lots of questions.

By the way, Dr. Yes, you beat me. I wondered where the 50% came from.

And was this guy trying to find indication of infection by looking in urine? Well, did he?

And did I see this guy is in allergy and asthma? So what's his connection to CFS? Why does he care?

I will say, he does seem to know a lot about biological abnormalities we have based on the questions he asks. But we already knew the questions and don't all the other researchers, I would think.

Tina
 

acer2000

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If this is the same guy that was looking at spinal fluid for various proteins in CFS, maybe he can go back and use those same samples and test from for evidence of XMRV infection?