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Sept 10: CDC 'conference call' including Unger and Lipkin

currer

Senior Member
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1,409
Infection, vaccines and other environmental triggers of autoimmunity.

Molina V, Shoenfeld Y.
Source

Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel.
Abstract

The etiology of autoimmune diseases is still not clear but genetic, immunological, hormonal and environmental factors are considered to be important triggers. Most often autoimmunity is not followed by clinical symptoms unless an additional event such as an environmental factor favors an overt expression. Many environmental factors are known to affect the immune system and may play a role as triggers of the autoimmune mosaic.Infections: bacterial, viral and parasitic infections are known to induce and exacerbate autoimmune diseases, mainly by the mechanism of molecular mimicry. This was studied for some syndromes as for the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and more. Vaccines, in several reports were found to be temporally followed by a new onset of autoimmune diseases. The same mechanisms that act in infectious invasion of the host, apply equally to the host response to vaccination. It has been accepted for diphtheria and tetanus toxoid, polio and measles vaccines and GBS. Also this theory has been accepted for MMR vaccination and development of autoimmune thrombocytopenia, MS has been associated with HBV vaccination. Occupational and other chemical exposures are considered as triggers for autoimmunity. A debate still exists about the role of silicone implants in induction of scleroderma like disease.Not only foreign chemicals and agents have been associated with induction of autoimmunity, but also an intrinsic hormonal exposure, such as estrogens. This might explain the sexual dimorphism in autoimmunity.Better understanding of these environmental risk factors will likely lead to explanation of the mechanisms of onset and progression of autoimmune diseases and may lead to effective preventive involvement in specific high-risk groups. So by diagnosing a new patient with autoimmune disease a wide anamnesis work should be done.

(anamnesis - recollection, ie ask the patient about their past)
 

currer

Senior Member
Messages
1,409
I don't want to drive this thread off-topic, but there are many papers at that link relating to this and having just read them I seriously doubt that ME is a natural disease. There is evidence to link even MS and RA onset to vaccinations and adjuvants are designed to do what seems to be found in ME, that the immune system is upgraded and activated.

This is not weirdo science but a serious concern and one that is already a matter of scientific concern, it is just that the research is not publicised.

Lipkin is looking for the infectious agent that causes ME but cant find one. We may then be asked to assume that an infection came along, caused ME and then was eradicated from the body. But vaccination has just that kind of effect.

Any theory of ME has to take into account the rise in numbers of those affected, which parallels the autism rise.
I wont persist in posting on this topic on this thread but there are other papers on the thread here for anyone who is interested. http://forums.phoenixrising.me/index.php?threads/andrew-wakefield-links-autism-to-cfs.24896/page-2
 

Forbin

Senior Member
Messages
966
Interesting preliminary results in general. What about this below, has it been discussed yet?

"Now, looking at these sample pools, we found a virus known as anellovirus. These come in three different types, known as Alpha, Beta and Gamma, a torque teno virus in three quarters of the samples. The sequence was quite variable. I cannot tell you that this is specific for Chronic Fatigue Syndrome. I really can’t tell you what this means."

http://www.mecfsforums.com/wiki/Lipkin_presentation,_CDC_Conference_Call_9/10/2013

Wikipedia says (citing PMID 20497515): "Anellovirus species are highly prevalent and genetically diverse. They cause chronic human viral infections that have not yet been associated with disease."

[Edit: another study found that "About 94% of healthy individuals in Russian population have more than 1000 TTV genome copies per 1 ml of blood.", so I guess it is ubiquitous.]

Yes, it's hard to tell what, if anything, to make of this. Did Lipkin find anellovirus in 75% of both patients and controls, or just in patients? I've seen general population prevalence rates of >50%, >90%, and the 94% rate mentioned above, but it is a recently discovered virus, so that may account for the wide range of estimates.

I did come across a 2012 paper that found that EBV stimulates torque teno virus (TTV) replication and postulates a possible connection to MS. TTV is a genera of anellovirus.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3285200/

I don't know if it's relevant to CFS in this case, but the general concept of one virus stimulating the replication of a completely different virus is interesting. I'm thinking in terms of perhaps multiple "indirect triggers" stimulating the replication of the actual "culprit."
 

Marco

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I don't know if it's relevant to CFS in this case, but the general concept of one virus stimulating the replication of a completely different virus is interesting. I'm thinking in terms of perhaps multiple "indirect triggers" stimulating the replication of the actual "culprit."

It does appear to be ubiquitous - infecting some 80% of the population and may be present from birth (or even pre-natally) and is a long-lasting infection. So far there hasn't been any confirmed association with any human disease but it does appear to amplify the production of pro-inflammatory cytokines (espec IFN-y) when there is a co-infection :

http://www.sciencedirect.com/science/article/pii/S0042682209005261

Another paper suggests anelloviruses have central nervous system effects - which would be interesting - but the full paper is behind a paywall.
 

Daffodil

Senior Member
Messages
5,875
very bad brain fog here; sorry my thoughts are not too cohesive.

ok so we have all heard about CFS clusters....and I think there have been MS clusters too, though not as many. now...how can clusters be explained if it is autoimmunity?

I have heard hundreds of reports of a spouse "giving" the disease to the other spouse....but I have heard of even more incidents where one spouse has it and the other is not even a little sick.

there are parents who seem to pass this on to offspring.

I heard that a transfer of a large number of white blood cells can pass on autoimmunity...but this does not happen through sex and I don't think it happens in childbirth....and it certainly cannot explain clusters.

so let's assume its the gut microbiome that makes one susceptible. now...since we inherit our microbiome, in part, perhaps that can explain autoimmunity that appears to get passed down...after years together, a couple will have a similar microbiome. people living in the same area might have the same microbiome due to environmental factors...

does this sound far-fetched? I don't know anymore.

there is a nurse who got this through a needle prick. did she have a messed up gut and get an infection....and then get CFS???
 

Legendrew

Senior Member
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Location
UK
ok so we have all heard about CFS clusters....and I think there have been MS clusters too, though not as many. now...how can clusters be explained if it is autoimmunity?

I have heard hundreds of reports of a spouse "giving" the disease to the other spouse....but I have heard of even more incidents where one spouse has it and the other is not even a little sick.

there are parents who seem to pass this on to offspring.

I heard that a transfer of a large number of white blood cells can pass on autoimmunity...but this does not happen through sex and I don't think it happens in childbirth....and it certainly cannot explain clusters.

so let's assume its the gut microbiome. now...since we inherit our microbiome, in part, perhaps that can explain autoimmunity that appears to get passed down...after years together, a couple will have a similar microbiome. people living in the same area might have the same microbiome due to environmental factors.....

so is this the answer?? is this starting to sound far-fetched to anyone?? I just don't know anymore.

what about the cases where people got CFS after a needle prick? I know of a nurse who got it this way from a CFS patient. if the patient had an autoimmunity, and the nurse also had messed up gut flora, what exactly was being passed in the needle prick???

bad brain fog here..sorry my comments are not more cohesive


Autoimmunity can account for a degree of clusters. Remember that all autoimmunity is thought to have a predisposed genetic component, this obviously can pass between families through generations. In a community it is fair to say that many members of individual families live in one community - this is changing today somewhat with the ease of travel but I still think it's a fair assumption to make that families tend to stick together. It 2-3 families in a community have this susceptibility and suddenly a virus able to trigger the predisposed immunity arises and sweeps rapidly through the community then you have what appears to be an outbreak. Because the predisposed genetic component elicited no symptoms the obvious thing people do is blame the virus and hence we have 30+ years of virus hunting - this have never bore any fruit however which has to tell you something with regards to ME.

As an analogy I believe the genetic predisposition is like have petrol liberally doused over an area - it's invisible (but likely a few small hints that go unnoticed) - it then only takes a spark in the form of a viral or bacterial trigger to start the immune activation and through exploitation of the genetic predisposition and suddenly a whole fire breaks out - this is when the symptoms first appear and suddenly it becomes much more difficult to manage. There is little point in identifying the initial virus or bacterial 'spark' as this does nothing to ease the fire. The only option then comes in calming the aberrant immune response and trying to break the autoimmune cycle.

I believe that the gut microbiome is an interesting area to explore and well worth a look but don't rule out standard autoimmunity just yet - sometimes we have to get a little more devious to explain thing like clusters but I think it is the hypothesis that has the most credence lately. I believe the gut micobiome hypothesis is hinging on the idea of environmental factor a little too much which despite their constant references have yet to get any significant evidence to support them.

With regards to spouse-spouse transmission I think it is certainly an interesting area and is worth looking at in studies but i'm hard pushed to base any hypothesis on it due to the lack of scientific data on the subject. With the needle prick idea, i suspect the nurse was likely already predisposed to developing ME and some form of pathogen was passed through the needle.
 

aimossy

Senior Member
Messages
1,106
I think something happens to switch the immune system on. and then it stays stuck on. whether its from virus or bacteria protozoa etc. the gut has a big involvement with the immune system. it seems to me that the study is finding good quality information and going in good directions. autoimmune conditions can also be triggered by virus/bugs stress etc. just got to get the people doing the work money.
 

Gijs

Senior Member
Messages
690
Business as usual. Nothing has been found. Sound familiar to me. I think the cause of this disease will never been found. It is to complicated. Sorry. There is only one thing left: the gut. It would make sense because the gut microbe produces neurotoxines. If the problem is not in the gut i believe the only thing left is: autopsy!
 

Legendrew

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Business as usual. Nothing has been found. Sound familiar to me. I think the cause of this disease will never been found. It is to complicated. Sorry. There is only one thing left: the gut. It would make sense because the gut microbe produces neurotoxines. If the problem is not in the gut i believe the only thing left is: autopsy!


No viral cause has been found - the immuneological activation however I think is incredibly interesting and lends credence to either an autoimmune causation, as Fluge and Mella believe, or a more subtle form of infection, as Lipkin believes.
 

Overstressed

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Belgium
After quickly reading a transcript of the meeting, I think Dr.Lipkin might know what is causing disease, but didn't find proof. I can't help, but when you dismiss 85% of retrovirus found in the blood, you have to have a very good idea of what is going on. I think he has found somewhat of a blueprint of infection traces, perhaps a past infection(s)? Maybe that's the reason he wants to look at antibodies(past infection)? I think he can link this blueprint to typical behaviour of certain pathogen's, but didn't find the pathogen itself. Maybe in the gut?

It's just my interpretation. I find it striking that he minimizes the 85% retrovirus infection, and for doing that, he must have a very good alternative hypothesis. Other researchers might claim that a retrovirus is the causing agent in this very situation.

Best wishes,
OS.
 

Gijs

Senior Member
Messages
690
No viral cause has been found - the immuneological activation however I think is incredibly interesting and lends credence to either an autoimmune causation, as Fluge and Mella believe, or a more subtle form of infection, as Lipkin believes.

The immuneological activation is nothing new and there are subsets; like immunedisfunction or underactiveimmunerespons. It does not fit in the big picture. And the use for cytokine profile markers will not be accepted by the medical community, it never did. At this point the 'Lipkin study' leaves us with empty hands. In the next 5 years nothing will be found with leaves to a beakthrough. And maybe i am a little negative but i do not expect any beakthroughs at all, never in our lifetime. Lets say: 50 year. Sorry people.
 

Gijs

Senior Member
Messages
690
After quickly reading a transcript of the meeting, I think Dr.Lipkin might know what is causing disease, but didn't find proof. I can't help, but when you dismiss 85% of retrovirus found in the blood, you have to have a very good idea of what is going on. I think he has found somewhat of a blueprint of infection traces, perhaps a past infection(s)? Maybe that's the reason he wants to look at antibodies(past infection)? I think he can link this blueprint to typical behaviour of certain pathogen's, but didn't find the pathogen itself. Maybe in the gut?

It's just my interpretation. I find it striking that he minimizes the 85% retrovirus infection, and for doing that, he must have a very good alternative hypothesis. Other researchers might claim that a retrovirus is the causing agent in this very situation.

Best wishes,
OS.
You think to deep. Lipkin knows 'nothing'. Almost all people have some old retroviruses.
Healthy people too.
 

Legendrew

Senior Member
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541
Location
UK
The immuneological activation is nothing new and there are subsets; like immunedisfunction or underactiveimmunerespons. It does not fit in the big picture. And the use for cytokine profile markers will not be accepted by the medical community, it never did. At this point the 'Lipkin study' leaves us with empty hands. In the next 5 years nothing will be found with leaves to a beakthrough. And maybe i am a little negative but i do not expect any beakthroughs at all, never in our lifetime. Lets say: 50 year. Sorry people.


I think you have to be positive with these things - these markers of immune activation are nothing new as you say but don't forget that replication is often the name of the game. Through replication we will be able to understand which markers are consistent within the ME picture and hopefully this will help us understand the mechanism at the root of all ME. It may be disappointing to report no significant findings with regards to a virus but sometimes finding nothing is more important than finding what you set out for. The lack of consistent viral findings tell us that these are not at the root of the disease which means future studies can place less importance on these and hence narrow the search criteria. Indeed having empty hands lets you change your line of thought and research more easily than having hands full of disparate viral findings. These immune markers are not hugely significant but they are clues as to where to look in the future. When you combine these clues with other hints we've discovered along the way its clear to see that ME research has the best leads it has ever had - from a personal perspective I think ME research is turning the corner now.
 

akrasia

Senior Member
Messages
215
It is about action not words. CFS is very much a unique case, it is uniquely neglected for reasons that have not been fully explained. To be aware of the seriousness, but not take action that leads to change, is to be complicit in the continued disempowement of the CFS community.

Fauci is complicit. The NIH is complicit. Fauci is the architect of a policy of exclusion, denial and trivialization that is tantamount to a violation of a human right to appropriate medical treatment and by extension research commensurate with what is standard in a first world economy.

Most of the post was prologue to the suggestion that M.E. be moved from the nowhere of the Office for Research into Women's Health, which was created as a sop to women's issues by a deeply misogynistic NIH, back to the National Institute for Allergy and Infectious Disease.

The point of the post was to frame an issue that was not about money but about credibility.

It is worth a visit to the link posted by Ecoclimber, where the late Tom Hennessy, who took no prisoners when he spoke, recounts a conversation with Stephen Straus.

That's what we're up against at the NIH. The representative from the ORWH tells us we should be grateful for her services because she has to put up with insult and derision from her colleagues because this is her assignment.

Asking why Fauci, given that he can't deny that he's gotten the message of the seriousness of the illness, delivered by Lipkin who he's invested with high cognitive authority, won't allow M.E. back into the NIAID is a valid advocacy issue. It would be a small step but symbolically would possess great value. Just the act of doing it would be an acknowledgement of a terrible error.

.
 

Marco

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I think you have to be positive with these things - these markers of immune activation are nothing new as you say but don't forget that replication is often the name of the game. Through replication we will be able to understand which markers are consistent within the ME picture and hopefully this will help us understand the mechanism at the root of all ME. It may be disappointing to report no significant findings with regards to a virus but sometimes finding nothing is more important than finding what you set out for. The lack of consistent viral findings tell us that these are not at the root of the disease which means future studies can place less importance on these and hence narrow the search criteria. Indeed having empty hands lets you change your line of thought and research more easily than having hands full of disparate viral findings. These immune markers are not hugely significant but they are clues as to where to look in the future. When you combine these clues with other hints we've discovered along the way its clear to see that ME research has the best leads it has ever had - from a personal perspective I think ME research is turning the corner now.


I've no reason to, but I've suspected from the start that they didn't expect to find any specific active infections and were essentially 'going through the motions' as a means of clearing the decks to focus on more promising avenues.

Which may sound rather negative if not deceitful but I don't see it that way. It was entirely necessary in my view to conduct a large, robust and credible study to eliminate, beyond reasonable doubt, a single pathogen theory. Anything less would just not have been accepted in certain quarters.

Hopefully we can now move on from virus hunting.
 

Dolphin

Senior Member
Messages
17,567
here we have helped put money into professor tates, im sure they would all be keen all over the globe. how do I post that post onto the fundraising idea thread.im techno challenged, if anyone thinks its valid please feel free to grab this and copy to that thread.lol.

Well done Kiwis. :thumbsup:
 

Gijs

Senior Member
Messages
690
I've no reason to, but I've suspected from the start that they didn't expect to find any specific active infections and were essentially 'going through the motions' as a means of clearing the decks to focus on more promising avenues.

Which may sound rather negative if not deceitful but I don't see it that way. It was entirely necessary in my view to conduct a large, robust and credible study to eliminate, beyond reasonable doubt, a single pathogen theory. Anything less would just not have been accepted in certain quarters.

Hopefully we can now move on from virus hunting.

I agree. I am not optimistic at all. Especially not with the CDC study. One single day test CPET will 'proof' for them that the cause is deconditioning. There 'corrupt' because they do not want to pay insurance money etc.. They want to disapprove the Ness study. Believe me.