Dr Bieger and Dr Mikovits discuss treating ME patients with Rituximab

[A.B.]

99.999999% of the time if an antibody is made that binds to self the immune system sees that a mistake has been made and kills the B cell, or tells it to try again. But it seems that just occasionally the immune system fails to see the mistake. Interestingly, this only seems to happen with certain very specific anti-self mistakes like anti-IgG or anti-DNA or anti-thyroglobulin. You never seem to get anti-albumin or anti-actin or anti-caeruloplasmin etc. The explanation for this that Dr Cambridge and I have suggested, along with a lot of other people suggesting something similar, is that the mistakes get missed if the antibody is against something that already acts as an immune signal.

What kind of immune signal does thyroglobulin represent?

Wikipedia says that it interacts with binding immunoglobulin protein but I don't understand what this means.

 

[Marco]

Ok. Answer this for me. I smoke. I've got UC. Always puzzled me.

Unlucky you - if autoimmune disease is effectively random.

 

[rosamary]

Unlucky you - if autoimmune disease is effectively random.

Lol. It leaves me just wondering what to do! Give up the fags and the controlled UC comes back avec vengeance or don't disturb the waters.

 

[rosamary]

Lol. It leaves me just wondering what to do! Give up the fags and the controlled UC comes back avec vengeance or don't disturb the waters.

I am going to give the answer as I sense it will be:

Giving up the fags will not affect it at all.

I think it will gently carry on being quiescent as long as I take the drugs.

It's a strange one.

But that's my 'gut' feeling.

But it makes me wonder what is really going on with this autoimmunity stuff. My guess is it is hereditary.

Now I will shut up and reflect.

 

[Jonathan Edwards]

What kind of immune signal does thyroglobulin represent?

Wikipedia says that it interacts with binding immunoglobulin protein but I don't understand what this means.

Excellent question. And I do not have a good answer. Something like 20% or more of normal people have antibodies to proteins involved in thyroid hormone manufacture like thyroglobulin and thyroid peroxidase. It must be an easy mistake to make. The only thing I can think of is that lymphocytes have thyroxine receptors and antibodies that can recognise proteins involved in thyroxine synthesis might stick to thyroxine receptors that have thyroxine stuck to them. You can argue the shape interaction all sorts of ways, which makes the theory weak because there are too many possibilities. But it may be something along those lines. There are other diseases with autoantibodies to receptors on B cells (e.g. peanut agglutinin receptor in sarcoidosis).

The most obvious way of making the mistake of allowing an anti-self B cell to survive and make autoantibodies is for the autoantibodies to bind back on the B cells and give them a 'stay alive' signal. There are lots of potential examples of this. Binding to thyroxine receptors might fit - bt I have to say it is one of the ones I am least confident I understand.

 

[aquariusgirl]

I had posted and then deleted because at that point I had been too busy to read the thread. & I wasn't sure it was onpoint ..but perhaps my point bears making..

I was just wondering if it would be helpful for Professor Edwards to reach out to Dr Mikovits to discuss his concerns?

We have so few advocates....It would be nice to see them collaborate and co-operate where possible ...

And while I am on the subject, thanks for your input Professor Edwards!

 

[rosamary]

I had posted and then deleted because at that point I had been too busy to read the thread. & I wasn't sure it was onpoint ..but perhaps my point bears making..

I was just wondering if it would be helpful for Professor Edwards to reach out to Dr Mikovits to discuss his concerns?

We have so few advocates....It would be nice to see them collaborate and co-operate where possible ...

And while I am on the subject, thanks for your input Professor Edwards!

I am going to express my view on this. I know I don't post often and so I am an unknown quantity.

BUT: Professor Edwards has expressed his views which may upset many people. However, I did not detect anything other than a feeling that he felt duty bound to make his views clear. (Based on his expertise).

I don't feel he should 'reach out' .

However, having met dr mikovits, I feel that she is tough enough to 'reach in'.

So I think everyone will admire her if she does just that.

She is a scientist who has a lot to offer. (And a big heart) . And I, for one, will have immense respect for her if she takes this on board.

But I don't feel professor Edwards needs to 'reach out'.

I think they are both capable of turning this into something good and positive.

But, Dr mikovits, if you are out there , make contact and let's turn lemons into lemonade.

Right, I am off again to my world of optimism and hope.

Xx

 

[Sherlock]

[Judy Mikovits has] a big heart

From the little exposure of her that I've had from a few videos and audio interviews, I'd say that you are right in that. She's instinctively likeable because of it.

I did not detect anything other than a feeling that [Jonathan Edwards] felt duty bound to make his views clear.

I believe that's very correct also.

 

[dannybex]

Dr Mikovits has literally given her all to do just as you suggest, but how can she do that without a lab? It is the same old pattern; whenever a scientist promotes our cause history proves they are hounded out of the field.

Tell that to Nancy Klimas, Lucinda Bateman, David Bell, Cheney, Peterson, etc., etc., etc..

 

[Research 1st]

That's initially a good point there, but the people you list above didn't individually attempt to expose a retrovirus in CFS patents to the public as lead scientists. Klimas could have gotten involved, but backed away verbally confirming she would leave any discovery to others in a 'CFS' presentation on XMRV. She went from giving talks on XMRV to recommending everyone exercises. Quite peculiar.

This was a wise career move, as Whistle-blowers aren't tolerated by the state, be it vCJD, Autism, CFS, or GWS.

What we know now, since 2015, is human cell lines are contaminated with MLV at approximately 3.3%. This would mean that lab workers have been potentially spreading these to human populations since the 1950's at least.

Prevalence and Characterization of Murine Leukemia Virus Contamination in Human Cell Lines
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0125622

A CFS patient who has evidence of reverse transcriptase (RT), who is HIV and HTLV negative, likely has an active retrovirus infection of unknown cause. (RT in patients was demonstrated by Defreitas and Holmes decades ago).

Mikovits and DeFreitas were correct all along hence they are isolated, the story focusses away from one single line of investigation, and the single line of investigation fails (what a surprise!).

Alter's 2011 paper demonstrated antibodies to SFFV, which was called negative despite unanswered question potentially revealing approximately 10 million Americans may have a laboratory created infection.

The now retracted original 2009 'XMRV' paper demonstrated SFFV also. (Only part of the 2009 paper was on XMRV - Silverman's contamination). The other part, was conveniently ignored, because the people who potentially caused MLV's or variants,were government scientists researching cancer. It was also ignored as no whole virus was found, what science needs to be called 'a virus' obviously.

Having dying cancer patients, testing themselves for MLV like infections, would not go down very well, should they turn out positive. The same goes for MS, Parkinsons, Autism, CFS and of course, Lyme disease.

Rogue MLV genes may individually or in combination with other pathogens (EBV, Borrelia) activate HERVs, and the HERV's could theoretically cause the symptoms of 'ME' via autoimmunity attack against mitochondrial function, which won't show up on a muscle biopsy, as it is an immune driven dysfunction.

SFFV is a neurotoxin in mice. With a poor blood brain barrier (if you have no PrpC left), then these horrible pathogens, or genes may infiltrate brain tissue or alter nerve function in the brain.

It's much easier to blame the patient (via Fukuda CFS or Oxford CFS) and use 'fatigue' as the requirement to be a CFS and thus disbelieved and ignored. This started in 1988 and remains in 2015.

Proving infectious onset would have changed everything for ME sufferers, but allowing this would lead to a plethora of other conditions, some fatal, potentially becoming associated to these hybrid lab infections also An infection that potentially accidentally 'got out, but remains unproven either way.

 

[barbc56]

Klimas could have gotten involved, but backed away verbally confirming she would leave any discovery to others in a 'CFS' presentation on XMRV. She went from giving talks on XMRV to recommending everyone exercises. Quite peculiar.

I think it's actually very logical. The science was pointing in the other direction.

Is exercising really the only thing she recommends?

Maybe I need to catch up on what she's doing.

Barb

 

[Izola]

What kind of immune signal does thyroglobulin represent?

Wikipedia says that it interacts with binding immunoglobulin protein but I don't understand what this means.

Me, either. iz

 

[BurnA]

Is it just me or does this video scare the crap out of anyone else ? I mean if this Dr. is supposed to be some form of expert on ME/CFS what hope do we have ? Thank goodness @Jonathan Edwards is around these parts to ensure we dont get conned by some doctor because they sound authoritive.

 

[Jonathan Edwards]

What kind of immune signal does thyroglobulin represent?

Wikipedia says that it interacts with binding immunoglobulin protein but I don't understand what this means.

Sorry I missed this question.
This is a tricky one but the interesting thing is that we make autoantibodies to several thyroxine binding proteins - including thyroglobulin and thyroid peroxidase and whatever mediates thyroid stimulation in Graves disease. The suggestion we came up with is that the reason these proteins get involved in antibody mistakes is that thyroxine itself is one of several direct stimulants of B and T cells. Antibodies that bind thyroxine binding proteins (as thyroxine does) may mimic thyroxine and so bind to receptors on lymphocytes stimulating them like the thyroid gland.

One reason for thinking this is plausible is that antibody binding to other lymphocyte stimulating receptors like Toll like receptors is thought to be involved in driving antinuclear antibody production. other examples are antibodies to two specific lymphocyte receptors Peanut Agglutinin receptor (autoantibodies in sarcoidosis) and Conconavalin A receptor (antibodies in Crohn's disease).

Clearly there are all sorts of hypotheses one could build about these interactions and many will be off target. However, the basic fact that we only tend to make autoantibodies to about fifty proteins does seem to call for a general hypothesis of this sort.