German study finds xmrv

ixchelkali

Senior Member
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This report is meaningless, meaningless do you hear me?

Ha! Where does it give the age and gender distribution of the patients? And just where in northern Germany were they from, hm? Maybe there was a cluster there. And were the controls carefully matched in all ways except that they were healthy? Without knowing these things, the rate of XMRV infection means NOTHING!

Ducking for cover....




Sarcarm, Satire, Humor, Tongue-in-Cheek, Irony Sarcarm, Satire, Humor, Tongue-in-Cheek, Irony
 

Eric Johnson from I&I

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"because XMRV does its damage when inserted which is different to HIV and inserts into start sites of genes.it moves around the genome.If it inserts into a regulatory gene which regualtes 40 other genes then some consequences are virtually inevitable"

Insertion mutagenesis is not likely to be the proximal cause of CFS. What evidence whatsoever exists to that effect? The pathogenesis of CFS (if it is caused by XMRV) is many times more likely to hinge on the recently-discovered conserved potently-immunosuppressive region of the Env (or whatever protein that region was in). But it could easily be something else instead.
 

girlinthesnow

Senior Member
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273
We already know that a person can be XMRV+ and be asymptomatic. What happens next? I remember Dr Mikovits talking about 'insults' in an infected person. in an adult this could be a high stress event, inflammation caused by other infections or the cycling of sex hormones or a combination of all three triggers that turn on the virus, causing it to replicate. In children who are born XMRV + (vertical transmission), the addition of vaccines, which ramp up the immune system could be enough. Genetic defects may not be necessary to present symptoms of XMRV, to get ME or other related diseases. We don't know yet.

So an initial infection, then something happens to us, a car crash, a secondary infection, pregnancy, vaccines for foreign travel....... basically life happens and then we get ME.
 

leelaplay

member
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1,576
Hi Eric - I think the german paper is the one she meant. She said something like" 3 negative papers have come out since the original xmrv paper, and there is another positive one and another negative one coming soon."
 
G

Gerwyn

Guest
"because XMRV does its damage when inserted which is different to HIV and inserts into start sites of genes.it moves around the genome.If it inserts into a regulatory gene which regualtes 40 other genes then some consequences are virtually inevitable"

Insertion mutagenesis is not likely to be the proximal cause of CFS. What evidence whatsoever exists to that effect? The pathogenesis of CFS (if it is caused by XMRV) is many times more likely to hinge on the recently-discovered conserved potently-immunosuppressive region of the Env (or whatever protein that region was in). But it could easily be something else instead.

insertional mutagenesis within the regulatory genes of nfat and creb would change the reading frame of these genes which regulate numerous other processes in our bodies.we dont suffer from immunosuppression but immunomodulation.something is modulating our immune response and producing a characteristic cytokine signature well beyond the ingective stage when the virus is latent and env is not present
 

cfs since 1998

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761
Hi Eric - I think the german paper is the one she meant. She said something like" 3 negative papers have come out since the original xmrv paper, and there is another positive one and another negative one coming soon."

I hope that's not what she meant. The german paper isn't a confirmatory paper. It doesn't even have anything to do with CFS at all.
 

leelaplay

member
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1,576
I hope that's not what she meant. The german paper isn't a confirmatory paper. It doesn't even have anything to do with CFS at all.

I know - sorry. But for the first few minutes she gave an update on xmrv. The reference to an upcoming positive paper was in the mids of that at about one minute in I think.
 
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Gerwyn

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No i pointed out that you cant use logic you quoted figures which were based in false premesis and not in accordance with any observed facts.

According to your assumptions 0nly one in nine people with me would have the virus. I started from the basis of observed fact and pointed out the flaws in your assumptions which were erroneous.

Before presenting any scientific argument you must valdate your assumptions.If your conclusions are not fact then your argument is false.
 

dannybex

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insertional mutagenesis within the regulatory genes of nfat and creb would change the reading frame of these genes which regulate numerous other processes in our bodies. we dont suffer from immunosuppression but immunomodulation. something is modulating our immune response and producing a characteristic cytokine signature well beyond the ingective stage when the virus is latent and env is not present.

Gerwyn -- thanks for making this clarification. So many have described ME/CFS (or whatever you want to call it) as a result of a suppressed immune system. It's my understanding that the the top docs and studies have shown the immune system is dysregulated / imbalanced (a Th1/Th2 imbalance) / or modulated, as you say.
 

awol

Senior Member
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417
Gerwyn -- thanks for making this clarification. So many have described ME/CFS (or whatever you want to call it) as a result of a suppressed immune system. It's my understanding that the the top docs and studies have shown the immune system is dysregulated / imbalanced (a Th1/Th2 imbalance) / or modulated, as you say.

Danny, immune suppression does still play a role but needs to be differentiated from the actual immune system changes that are part of this disease. Immune suppression likely contributes to making us sick in the first place. It also contributes to worsening of symptoms after over-exertion. This is because when the body goes into a state of immune suppression for whatever reason, usually when working hard on other priorities, we are more likely to catch viruses and bugs, and they spread more easily. Latent infections can also be set loose when the immune system is suppressed.

The actual changes that have been observed in our immune systems are something else entirely, contributing to symptoms that are NOT caused by latent infections etc. and that continue even when our immune systems are not suppressed.
 
G

Gerwyn

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Danny, immune suppression does still play a role but needs to be differentiated from the actual immune system changes that are part of this disease. Immune suppression likely contributes to making us sick in the first place. It also contributes to worsening of symptoms after over-exertion. This is because when the body goes into a state of immune suppression for whatever reason, usually when working hard on other priorities, we are more likely to catch viruses and bugs, and they spread more easily. Latent infections can also be set loose when the immune system is suppressed.

The actual changes that have been observed in our immune systems are something else entirely, contributing to symptoms that are NOT caused by latent infections etc. and that continue even when our immune systems are not suppressed.

Hi AWOL.OUR cytokine pattern is actually consistent with a latent virus infection.The corticosteroid pattern produced by this cytokine signature would make us more prone to secondary infection by further suppressing TH1 activity. This can cause enough problems to enable a virus like xmrv to leave latency which means that it could"infect" more and more genes
 

awol

Senior Member
Messages
417
Hi AWOL.OUR cytokine pattern is actually consistent with a latent virus infection.The corticosteroid pattern produced by this cytokine signature would make us more prone to secondary infection by further suppressing TH1 activity. This can cause enough problems to enable a virus like xmrv to leave latency which means that it could"infect" more and more genes

ok, yeah that too. :)

I guess what I meant is that immune suppression is a normal thing that happens from time to time to everyone and does not mean you are sick. Continuous abnormalities and changes in ME/CFS are something else (like a retrovirus maybe).
 

Eric Johnson from I&I

Senior Member
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337
It's true that the great majority of us seem unlikely to have any gross immune suppression. But even if one little branchlet of immunity (one cell type, or whatever) were seriously impaired, that might in some people permit ubiquitous organisms like Chlamydia pneumoniae or HHV6 to reach equilibrium densities in tissue that are say 100x higher than are found in normals. It's simple to imagine this creating non-progressive neuroinflammation, which might well be what CFS is.

Of course, CFS might also sometimes involve low-grade peripheral inflammation too -- or, as far as I can tell, it might not. I can't think of any symptom that couldn't possibly be CNS-mediated.
 

awol

Senior Member
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417
It's true that the great majority of us seem unlikely to have any gross immune suppression. But even if one little branchlet of immunity (one cell type, or whatever) were seriously impaired, that might in some people permit ubiquitous organisms like Chlamydia pneumoniae or HHV6 to reach equilibrium densities in tissue that are say 100x higher than are found in normals. It's simple to imagine this creating non-progressive neuroinflammation, which might well be what CFS is.

Of course, CFS might also sometimes involve low-grade peripheral inflammation too -- or, as far as I can tell, it might not. I can't think of any symptom that couldn't possibly be CNS-mediated.

Impaired immune function is not the same thing as suppression. We have to clear up the confusion.
 

garcia

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It's true that the great majority of us seem unlikely to have any gross immune suppression. But even if one little branchlet of immunity (one cell type, or whatever) were seriously impaired, that might in some people permit ubiquitous organisms like Chlamydia pneumoniae or HHV6 to reach equilibrium densities in tissue that are say 100x higher than are found in normals. It's simple to imagine this creating non-progressive neuroinflammation, which might well be what CFS is.

Hi Eric, I agree with all the above, except the "non-progressive" bit. My neuroinflammation feels very progressive to me! I haven't managed to make a dent in my Cpn infection after 3 years of trying, I strongly suspect due to XMRV immunosuppression. I'm sticking with the word suppression, since it is the word commonly used (e.g. "retroviruses cause immune suppression").
 

lansbergen

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2,512
Impaired immune function is not the same thing as suppression. We have to clear up the confusion.

It is important to know the difference. Can you give definitions?

Years ago I said whatever the agent is, it disturbs the immune system. On the one hand it is working like hell and on the other hand it fails to do what it always did before the problems started .
 

awol

Senior Member
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417
I'm sticking with the word suppression, since it is the word commonly used (e.g. "retroviruses cause immune suppression").

Your choice, but this is a mistake that adds to the confusion.

Saying with one sweeping statement that retroviruses cause immune suppression is premature in the case of xmrv because we don't know exactly what it does to the immune sytem yet. Normally, when you have a viral infection, the immune system is ACTIVATED, not suppressed. However xmrv may be causing changes to our immune systems that make the normal immune response ineffective, even while active. This is dysfunction, not suppression.

Suppression is what happens when you are healthy, and working hard. For example, you are running a marathon (he he, once upon a time). Because you are exerting yourself, your cortisol levels go up. When cortisol is elevated, the immune system is suppressed. But you are running a marathon. You are perfectly healthy. It is just that your body has to adjust to the high demand placed on it so the immune sytem gets lower priority temporarily. This is immune suppression.

What happens with HIV is immune DEFICIENCY not suppression. Transplant patients have their immune sytems deliberately suppressed with medications and steroids so that they don't reject the new organs. This does not mean that their immune system does not work. Once the intervention stops their immune system will be fine.

What we have is something else again. Our systems are both overactive and impaired. This is seen by researchers as very very strange. There is no doubt that there is a problem with our immune response. But this is NOT the temporary and perfectly normal process of immune suppression caused by raised cortisol in response to exertion. Nor is it the deliberate intervention that is done for transplant patients so that their organs are not rejected.
 
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