Tweets from Invest in ME conference

[Daffodil]

DeBortgjemte (English & Norwegian) and JAScarb

MLV/XMRV Lipkin study to be out June 30

Rituximab given every 20 weeks, remission in 2/3

 

[SilverbladeTE]

Lipkin study finds that ME is caused by Bullshitus Moronii Wesselry, a colon dwelling HG retrovirus!

 

[Sasha]

Thanks, Daffodil - here is the link to journalist Jorgen Jelstad's twitter feed from the conference - it's very interesting. He's tweeting both in Norwegian (?) and English, which is very thoughtful of him!

The conference sounds excellent. I'm looking forward to hearing more detail.

I just had a quick look at his blog on Wordpress - he's written a book about ME, and his interest is due to his mother having ME.

 

[acer2000]

Is it just me, or does all this talk about ME/CFS being "autoimmune" making anyone else nervous? How does autoimmunity explain clusters and transmission? I appreciate the fact that they are getting a lot of funding and useful info out of studies following the rather serendipitous discovery that Rituximab effects the symptoms of ME. But just because Rituximab helps the symptoms of some people with ME, doesn't mean that ME is autoimmune by nature. Likewise, just because scientists can observe that the immune system is active in ME patients and they have yet to find a pathogen to explain this doesn't mean its by default "autoimmune". Just think, if that were the case, researchers would have declared pretty much much every infectious disease ever discovered in history "autoimmunity" on account of their ability to detect an immune response in patients before they even started looking for the root pathogen causing the response. Come on guys, don't give up and call it the immune response "autoimmune" - you haven't even really started looking for the cause yet.

 

[acer2000]

From the twitter feed:

#MELondon Mella: Done immune measurments during treatment at several time points. No changes in NK or T-cell numbers

Does that mean that the low NK cell function and abnormal T cell counts didn't normalize on Rituximab? (bad)? Or does that mean they didn't get worse on the treatment (good)? If the former it would seem to mean its beating back the symptoms and not the disease (much like steroids would). If the later I guess thats a good sign. I hope they circle back and try to figure out whats going on here.

 

[Guido den Broeder]

How does autoimmunity explain clusters and transmission?

It doesn't. The clusters are explained by the trigger, i.e. the enterovirus. The autoimmunity is our disfunctional response to the trigger, where the disfunctionality is caused by the latent herpes virus (and our genetic material that it uses).

 

[Guido den Broeder]

From the twitter feed:

#MELondon Mella: Done immune measurments during treatment at several time points. No changes in NK or T-cell numbers

Does that mean that the low NK cell function and abnormal T cell counts didn't normalize on Rituximab? (bad)?

Counts are not the same as abnormalities. Rituximab targets B cells. The body will replenish the B cells but the new ones will hopefully function correctly.

After that, the body still has to combat all active infections, and that will take time. But it should then be far more effective.

 

[acer2000]

It doesn't. The clusters are explained by the trigger, i.e. the enterovirus. The autoimmunity is our disfunctional response to the trigger, where the disfunctionality is caused by the latent herpes virus (and our genetic material that it uses).

OK then, lets say I accept that premise. But then how do you explain how a group of completely non (genetically) related people have the same persistent dysfunctional response to a common pathogen at the same time? Its seems like it might be likely that several people in the same family might react in the same dysfunctional way to a common pathogen. But not a whole town of unrelated people - unless there was another unique circumstance (pathogen, environmental exposure, etc..) shared between them - which is why I posed the question.

 

[acer2000]

Counts are not the same as abnormalities. Rituximab targets B cells. The body will replenish the B cells but the new ones will hopefully function correctly.

After that, the body still has to combat all active infections, and that will take time. But it should then be far more effective.

Understood, but low (NK) counts *and* abnormalities in function have been described in ME/CFS. As well as high T cell counts in some papers. If Rituxan is addressing the root cause of ME/CFS, wouldn't you expect all of these things to come in line? Which is why I was asking for clarification on what that tweet meant.

 

[Guido den Broeder]

Not before quite a while after the treatment, and of course only if the treatment is succesful. You'll feel better much earlier though. I'd think that even with relatively low NK response you can overcome remaining infections once the signals are no longer off. But the metabolism itself can take longer to rebalance, and parts of it may never quite return to normal.

OK then, lets say I accept that premise. But then how do you explain how a group of completely non (genetically) related people have the same persistent dysfunctional response to a common pathogen at the same time? Its seems like it might be likely that several people in the same family might react in the same dysfunctional way to a common pathogen. But not a whole town of unrelated people - unless there was another unique circumstance (pathogen, environmental exposure, etc..) shared between them - which is why I posed the question.

Genetics alone can indeed not explain an epidemic nature of ME. That's why something like a herpes virus must be the cause of the bad reaction. And the staff of a hospital, or a school, or soldiers on expedition, are more likely to have shared a previous herpes infection. You will probably find this in all known outbreaks.

 

[acer2000]

Not before quite a while after the treatment, and of course only if the treatment is succesful.



Genetics alone can indeed not explain an epidemic nature of ME. That's why something like a herpes virus must be the cause of the bad reaction. And the staff of a hospital, or a school, or soldiers on expedition, are more likely to have shared a previous herpes infection. You will probably find this in all known outbreaks.

Yeah I guess, but millions of people have been exposed to/harbor latent herpes viruses. Not all of them get ME. In fact the vast majority of them don't, despite being exposed to other things that have been known to trigger ME. Thats why it seems to be that there is a novel intervening factor.

 

[Guido den Broeder]

True. Some factor X must explain why certain people with latent herpes develop ME upon getting infected with an enterovirus, while others perhaps get MS and yet others have no lasting problems at all.

Also, there are no known outbreaks of ME before 1934, and endemic cases were not described until a decade or so later. Something must have changed. Like new retroviral material, added to our DNA, for the herpes virus to play with.

 

[merylg]

There are at least 57 genetic links to MS that have been found....80% of those are Immunological...interesting...http://www.msrc.co.uk/index.cfm/fuseaction/show/pageid/1347