Mono Virus Discovery - Implications for ME/CFS?

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Cincinnati Children's Hospital just patented a system for transcription factor modification to treat autoimmune diseases. Here is a youtube video about the problem:


And here is the patent that (maybe?) helps treat the issue described in the above video:

Abstract: "Disclosed herein are methods of treatment of various disease states in which an individual in need thereof if administered one or more therapeutic agents capable of modulating one or more transcription factors. Also disclosed are methods by which an individual may be treated for one or more disease states, in which loci in which transcription factors bind are detected."

http://appft1.uspto.gov/netacgi/nph...srchnum.html&r=1&f=G&l=50&s1=20180016314.PGNR.

For some reason I can't add a period on the end of this link. If you add a period, then the link works.

Here is a quote from reddit about the patent:

"They basically patented the ability to use specific drugs to target specific transcription factors and to treat dozens of different diseases. They found associations with the levels of various different transcription factors and the diseases and identified ways that modifications to them can affect the genes that are implicated in the disease. Whether of not that actually affects the disease process, or is even a viable or safe technique in living cells, let alone patients, is still up for question but it provides a new avenue for exploration.

The video I linked to above identifies one such transcription factor that they found was not native to humans and through association studies they were able to link it to Epstein Barr Virus. They haven't actually published that paper yet so I don't know how they managed to prove that association or to understand exactly how key the EBNA2 gene is to the pathogenesis of the autoimmune diseases they identified. EBNA2 has not really been studied by anyone else before so this is totally new ground.

The entire idea of transcription factor modification has been around for a while but nobody has identified any real targets until now."

There is almost no chance that EBV effects these autoimmune diseases but not ME/CFS in a similar way. Maybe even more-so, due to the strong relationship between getting mono and ME/CFS.

Can someone show this to Dr Davis et all?
 
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That video is amazing. (And I say this as a person who has never before resorted to coloured fonts)

We always talk about a virus coming in and doing *something* that ruins us for ever more. And now we have a very strong candidate for what that something might be! Turning on genes that it shouldn't.

Here's a quote about lupus from a press release on this by the NIH.

“We were surprised to see that nearly half of the locations on the human genome known to contribute to lupus risk were also binding sites for EBNA2,” said Dr. Harley. “These findings suggest that EBV infection in cells can actually drive the activation of these genes and contribute to an individual’s risk of developing the disease.”


Great find.

I have no doubt OMF would be all over this.
 

Gingergrrl

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Epstein-Barr virus protein can “switch on” risk genes for autoimmune diseases
EBV may trigger some cases of lupus, say NIH-supported researchers.

https://www.nih.gov/news-events/new...ein-can-switch-risk-genes-autoimmune-diseases


Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity

https://www.nature.com/articles/s41588-018-0102-3


'Mono' virus linked to seven serious diseases
Epstein-Barr virus may affect health in more ways than known


https://www.sciencedaily.com/releases/2018/04/180416121606.htm
 
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From Science Daily https://www.sciencedaily.com/releases/2018/04/180416121606.htm

Software behind discoveries to be made public


Detecting and tracking the activities of these transcription factors took years of work involving dozens of laboratory and computational experts.

The project required gathering massive sets of genetic data, then analyzing every genetic change affecting the activity of the virus. Doing this required creating two new algorithms, called RELI and MARIO, which were developed at Cincinnati Children's by Weirauch and colleagues.

Both software tools and a related website will be made publicly available.

"We are going to great lengths to not only make the computer code available, but all of the data and all of the results," Weirauch says. "We think it's an interesting approach that could have implications for many diseases, so we're contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow up on them."
 
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Seems like they have figured out a genomic technique to see where in the genome the virus particle are affecting. I can see two ways this works to speed the understanding of MECFS for us.

One: they look at all the known genetic mutations that align with me/cfs (I believe Neil McGregor has a long list!) and look to see if they are attacked by any transcription factors from ebv.

Two: look at where the ebv transcription factors go then check patients to see if any of these are associated with me/cfs. Later, they should look to see if any other me/cfs associated viruses attack the same spots in the genome. If so, we have serious candidate genes.

Once we figure out which genes are acting up, we might be able to design better treatments.
 

Wonkmonk

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This is really interesting. I have long had the suspicion that a lot of the negative consequences of chronic stress is due to the impaired ability of the body to control herpes virus reactivations. CFS - in some patients - might be an extreme case of herpes viruses (mainly EBV) getting out of control and triggering all sorts of bad events.

This sheds some new light on @Gingergrrl's theory that her (confirmed) mono first triggered CFS and after years of positive IgM triggered a whole bunch of autoimmune problems. The study here seems to lend some support to this interpretation.

The pivotal question would be in how far these effects can be undone by better controlling the herpes virus. This could be the reason why Dr Lerner and Dr Montoya's methods help some patients, but long-term treatment is needed.
 

anni66

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This is really interesting. I have long had the suspicion that a lot of the negative consequences of chronic stress is due to the impaired ability of the body to control herpes virus reactivations. CFS - in some patients - might be an extreme case of herpes viruses (mainly EBV) getting out of control and triggering all sorts of bad events.

This sheds some new light on @Gingergrrl's theory that her (confirmed) mono first triggered CFS and after years of positive IgM triggered a whole bunch of autoimmune problems. The study here seems to lend some support to this interpretation.

The pivotal question would be in how far these effects can be undone by better controlling the herpes virus. This could be the reason why Dr Lerner and Dr Montoya's methods help some patients, but long-term treatment is needed.
Interesting software, but proteins binding to molcules does not mean that they are causative
 

Hip

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Quoting the article:
The study shows that a protein produced by the Epstein-Barr virus, called EBNA2, binds to multiple locations along the human genome that are associated with these seven diseases.
It looks like thymoquinone from the health supplement black seed oil (Nigella sativa) is particularly efficient at suppressing Epstein–Barr virus nuclear antigen 2 (EBNA2) protein, as well as LMP1 and EBNA1, at least in vitro.



As a dormant, non-active infection, Epstein-Barr virus can exist in one of 3 latency states. In the EBV latency I and latency II states, the virus does not produce EBNA2. However, in the EBV latency II state, the EBNA2 protein is synthesized by the virus.

This means that you do not have to have an active infection with EBV in order to be negatively affected by EBNA2, because even in latency, the EBNA2 protein can be manufactured.

According to Wikipedia, when EBV infects B-cells, it can enter the latency III state (one can thus speculate that destroying EBV-containing B-cells may be one mechanism by which rituximab ameliorates autoimmune disease).
 
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Tammy

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There is almost no chance that EBV effects these autoimmune diseases but not ME/CFS in a similar way. Maybe even more-so, due to the strong relationship between getting mono and ME/CFS.
I for one am happy that EBV is getting more and more attention. I believe it is the main culprit behind CFS and autoimmune. I have learned ALOT about this from Anthony William Medical Medium. (I realize most don't believe in this sort of thing).......His first book explained so much about EBV that I had never heard before.
 

Gemini

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"We are going to great lengths to not only make the computer code available, but all of the data and all of the results," Weirauch says. "We think it's an interesting approach that could have implications for many diseases, so we're contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow up on them."
@Janet Dafoe (Rose49) any way to reach out to these researchers who seem to be searching for collaborations?
 

Learner1

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Thank you for helping to find a link with the tables and images. However, this link didn't show the content - is there a correction perhaps?
 

Gingergrrl

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This sheds some new light on @Gingergrrl's theory that her (confirmed) mono first triggered CFS and after years of positive IgM triggered a whole bunch of autoimmune problems. The study here seems to lend some support to this interpretation.
Thanks @Wonkmonk but I cannot take any credit b/c none of it was my theory vs. what my ME/CFS and MCAS doctors told me. They both felt that (in my case) the EBV eventually shifted into autoimmunity. Initially I had severe (confirmed) Mono from EBV and when I got sick again ten months later, it was a viral illness and I had some kind of post-viral fatigue syndrome with POTS. The EBV stayed IgM+ for years at very high numbers until it finally went down and instead I had severe allergic reactions/anaphylaxis/MCAS and then all of these crazy autoantibodies.

My doctors both feel that if I ever become positive for EBV on a PCR test, I should go back onto an anti-viral, not for symptom relief, but to stop the EBV from replicating so it does not make the autoimmunity worse or lead to a re-activation of Mono, or even lead to cancer. They both take EBV very seriously and feel that it can lead to autoimmunity. So it is thrilling to see researchers, like Cincinnati Children's Hospital, backing this up.

According to Wikipedia, when EBV infects B-cells, it can enter the latency III state (one can thus speculate that destroying EBV-containing B-cells may be one mechanism by which rituximab ameliorates autoimmune disease).
My doctors agree with this, too, that (one mechanism) of Rituximab in autoimmunity is destroying the B-cells that contain EBV. I do not know what role this plays in my case vs. just destroying the B-cells that create the autoantibodies itself.
 
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Thanks @Wonkmonk but I cannot take any credit b/c none of it was my theory vs. what my ME/CFS and MCAS doctors told me. They both felt that (in my case) the EBV eventually shifted into autoimmunity. Initially I had severe (confirmed) Mono from EBV and when I got sick again ten months later, it was a viral illness and I had some kind of post-viral fatigue syndrome with POTS. The EBV stayed IgM+ for years at very high numbers until it finally went down and instead I had severe allergic reactions/anaphylaxis/MCAS and then all of these crazy autoantibodies.

My doctors both feel that if I ever become positive for EBV on a PCR test, I should go back onto an anti-viral, not for symptom relief, but to stop the EBV from replicating so it does not make the autoimmunity worse or lead to a re-activation of Mono, or even lead to cancer. They both take EBV very seriously and feel that it can lead to autoimmunity. So it is thrilling to see researchers, like Cincinnati Children's Hospital, backing this up.



My doctors agree with this, too, that (one mechanism) of Rituximab in autoimmunity is destroying the B-cells that contain EBV. I do not know what role this plays in my case vs. just destroying the B-cells that create the autoantibodies itself.
In the 10 month interval between mono and your other viral illness did you have major ME/CFS symptoms?

My case seems fairly similar. I had a bad case of mono and fully recovered. About 7 months later I developed an unknown viral illness (could have been reactivated EBV, but who knows) which brought the ME/CFS symptoms.
 

rel8ted

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Have always thought Mono (EBV) to be the main culprit of ME. I was perfectly healthy and active,and in bootcamp when I came down with Mono and have never been the same since. Within a year, I injured my leftl eg in a required run and the only thing I can remember about the incident is that I felt very weak and woozy and the next thing I knew 2 guys were carrying me. That feeling turned out to be the same alarm that my body uses to say,"hey, stupid, you've done way too much, we're shutting you down" to this day. I've tried a time or two since then to push beyond that, but it has never ended well. I don't enjoy waking up looking at scared faces staring back at me, so I have learned to listen.

Found it very interesting that inflammatory arthritis and Celiac were included in the very likely to caused by EBV category, I am the not-so-proud owner of those. Also was suspect for Lupus & MS but ruled those out and was DX with ME at the Charlotte clinic. I have always been highly suspect that ME has an auto-immune component and that it started with EBV.