EBV targeting treatment yields clinical improvements in spms

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Re: EBV targeting treatment yields clinical improvements in

Postby CureOrBust » Wed Nov 04, 2015 3:32 am

Thanks. Nope, I don't think I have seen this article before, or I just skim read it :oops: in favor of the actual published article.
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Re: EBV targeting treatment yields clinical improvements in

Postby PointsNorth » Sat Nov 21, 2015 4:21 pm

Pender got funding and his trial is underway. Can't find the link. I am going to try to tackle EBV using low dose immunotherapy this week.

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My Current Regimen http://www.thisisms.com/forum/regimens-f22/topic25634.html
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Re: EBV targeting treatment yields clinical improvements in

Postby Scott1 » Sat Nov 21, 2015 7:41 pm

Hi,

I'm not sure what you mean by low dose immunotherapy? If the plan is to target EBV then you need to understand what it is doing. It's not just the points that Pender makes. If you don't allow for what happens to an EBV infected B cell I imagine you will be disappointed.

As a shortcut: an EBV infected B cell is a prolific producer of superoxide. If this leads to the excessive production of peroxynitrite then glyceraldehyde-3-phosphate will be disabled and you will be unable to complete the most efficient method of making ATP. This will deplete your energy levels and lower your uric acid (which is neuroprotective). Its not hard to fix. Just take big doses of Q10 and acetyl-L-carnitine.
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Re: EBV targeting treatment yields clinical improvements in

Postby PointsNorth » Sun Nov 22, 2015 3:27 pm

Nice overview of low dose immunotherapy/allergy
MD in Alaska has taken low dose allergy to treating people with autoimmune disease.

http://imcwc.com/html5-blank/low-dose-a ... a-therapy/

I've Tested negative for Lyme disease but have used LDI for Lyme and experienced increased strength in legs and reduced fatigue. The doctor in Alaska believes that MS is simply a manifestation of Lyme disease. All his MS patients respond to the Lyme disease Low dose immunotherapy. The same patients respond equally as well to MBP Myelin basic protein. I get no benefit from MBP. I am going to try more antigens.
Albany 2010. Brooklyn 2011
Hayes inspired Calcitriol+D3 2013-2014
Coimbra Protocol 2014-16
DrG B12 Transdermal Spray 2014-16
Progesterone 2015-16
Low-Dose Immunotherapy 2015-16
My Current Regimen http://www.thisisms.com/forum/regimens-f22/topic25634.html
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Re: EBV targeting treatment yields clinical improvements in

Postby Scott1 » Sun Nov 22, 2015 4:12 pm

Hi,

I still don't understand what you mean by low dose immunotherapy. If your doctor believes MS is Lyme then he needs to get out more.
Understanding what the therapy is will help if Lyme is not a causative agent. I also don't know what you mean by antigens.

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Re: EBV targeting treatment yields clinical improvements in

Postby leonardo » Mon Dec 07, 2015 12:40 pm

Gammaherpesvirus Infection of Human Neuronal Cells

"To date, no in vitro study has demonstrated gammaherpesvirus infection of neuronal cells. Moreover, worldwide clinical findings have linked EBV to neuronal pathologies, including multiple sclerosis, primary central nervous system lymphoma, and Alzheimer's disease. In this study, for the first time, we have successfully demonstrated the in vitro infection of Sh-Sy5y and Ntera2 cells, as well as human primary neurons. We have also determined that the infection is predominately lytic."


http://www.ncbi.nlm.nih.gov/pubmed/26628726
http://mbio.asm.org/content/6/6/e01844-15.full
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Re: EBV targeting treatment yields clinical improvements in

Postby Scott1 » Mon Dec 07, 2015 2:03 pm

Hi,

It has been known for decades that EBV infected B cells are prolific producers of superoxide (EBV generally resides in B cells)
http://www.ncbi.nlm.nih.gov/pubmed/2849588
When in close proximity in Nitric Oxide they form peroxynitrite.
This is a cause of oxidative stress
http://link.springer.com/article/10.100 ... -z#/page-1

NO, O2 and ONOO- are all gases

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Re: EBV targeting treatment yields clinical improvements in

Postby DrGeoff » Mon Dec 07, 2015 2:28 pm

Way back on Page 1 of this thread, gainsburg wrote:
"The mere presence of the herpes virus somehow stimulates the immune system to attack the healthy tissue where the dormant herpes resides, ie. nerve tissue. "

This view line up with that of Murray (2005), that EBV and/or some other viruses are the triggers for MS. In fact, Murray covers EBV in several places
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Re: EBV targeting treatment yields clinical improvements in

Postby CureOrBust » Mon Dec 07, 2015 10:59 pm

Scott1 wrote:I've lost track of where I read it but somewhere in PubMed there is a mathematical model that concludes it would take Valacyclovir 11.3 years to clear EBV. Having pursued that route, I think it might take longer but the benefit was obvious in the short term for me. Of course, everyone will have their own metabolic state so it might take longer for someone else and it is clearly a very long term strategy.
Have you continued to use Valacyclovir (with a Y :wink: ) ? have you tried adding any other anti-virals? such as Raltegravir? (as used in the Charcot project?
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Re: EBV targeting treatment yields clinical improvements in

Postby Scott1 » Tue Dec 08, 2015 3:00 am

Hi,

I've stuck with Valacyclovir because for me it works. It is specific to herpes family viruses so it should work for EBV.
It obvious from other peoples experience that it isn't for everyone but I don't quite know why.

In my own case I aborted a trial of Biotin after 1 dose because of the way I felt but couldn't stop thinking if it was similar to the way others felt when they tried Valtrex. I suppose I am a little suspicious of interactions.

If I was starting from a fresh beginning I would try it on its own a slowly add any other supplements one at a time and think about how I felt before I broadened my intake. From memory, Anonymoose struggled with Valtrex and I think she concluded it was other supplements that were interacting.

So I think very highly of Valacyclovir but I wonder a lot about interactions that just have never been reported. Few are as adventurous as us.

It is easy to assume that what is harmless in others in safe for us.

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Re: EBV targeting treatment yields clinical improvements in

Postby CureOrBust » Mon Dec 14, 2015 4:24 am

Scott1 wrote:I don't know how the dosages were determined either. I've lost track of where I read it but somewhere in PubMed there is a mathematical model that concludes it would take Valacyclovir 11.3 years to clear EBV.
I stumbled across this study, which may be the one you are referring to.

http://jvi.asm.org/content/83/22/11857.full.pdf+html
EBV can be eliminated from the body in some patients after bone marrow transplantation (10). Based on the half-life of EBV in patients treated with valacyclovir and assuming that valacyclovir acts similarly on B cells in tissues as it does in the blood, we estimate that it would take 6 years of 500 mg of valacyclovir once each day to eradicate 99% of EBV from the B-cell compartment and 11.3 years to eliminate the virus completely from the body if persons were not reinfected during this time.
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Re: EBV targeting treatment yields clinical improvements in

Postby 1eye » Mon Dec 14, 2015 9:07 am

Sometimes I need to remind myself of how relieved I was when I was diagnosed with MS. Up until that my worst problem was that doctors thought I was a hypochondriac. The body is mysterious and doctors are wrong more than 50% of the time. Just ask Canadian broadcaster Dr. Brian Goldman.

In this talk he explains what a batting average is, and why we don't use percent for this statistic.

https://www.ted.com/talks/brian_goldman_doctors_make_mistakes_can_we_talk_about_that?language=en

It matters more when life is at stake and doctors sometimes hasten death. Hope they don't hasten yours. But if a batting average is as good as 400, you can be pretty sure the batter makes as few mistakes, or fewer, in less important, less life-threatening areas. Well to remember that is the same as 40%, and to wonder what happened the other 60. And what about the times your life did not hang in the balance. And what about the 60%+ of those times he did not hit safely?

In July of 2014 I fell backwards into a door frame (it was broken but got fixed). I broke my collar bone. I was on a road trip so my doctor was relied on by some emergency doctors to take care of me when I got home. He did have me x-rayed but nothing further was done. Apparently there are some big blood vessels around the collar bone and if you haven't messed these up, you will not find a GP willing to set a collar bone.

About a month ago I re-broke it, and it has been getting worse since then. I did not know what was wrong. I had fallen, but I had been OK fairly quickly.

Two days ago I took a very bumpy ride in a van to get it x-rayed. I was lucky to be seen on a Saturday. The radiologist must have known by how sick I acted. The drug store was on the way home. I have been taking strong painkillers since then. They phoned this morning to tell me to use a sling (it doesn't work) because apparently it has been re-broken. So that's why I had all this "nerve" pain. I really really want to see an orthopedic guy and maybe have it set (that's what fluoroscopes are for).

Lying down is the only position it doesn't hurt (much). Blood vessels may indeed be involved and the doctor I saw asked me to buy a good blood pressure machine.

BTW don't worry about 300 mg biotin. I didn't use filler until the last batch, so I was taking 300-500 mg before. It is odorless, tasteless, and the best effect it has had on me is to make my lower digestion work perfectly, even now when I am on massive opioids. I have postponed, and may cancel altogether, my colonoscopy. No one has said a word to me about the microbiota transplant I asked for. I think I will not be able to get it.

If it were my wife we would have both suspected a broken bone, as she has had many and knows what it feels like. She has osteopoenia. I have never broken a bone before, though I cracked an ankle once. I had been off it in a body cast for six months, and I was twelve. 12 to 61 without a break is pretty good.

Had I been seeing a neurologist for this I'm sure it would have been called neuropathic pain. Be careful with marrow transplants. My brother cannot leave his bed. He has serious host-graft disease, and it came with a bad bad case of shingles. He gets intravenous Lanacaine. I have had my shingles shot (but not flu yet this year).
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Re: EBV targeting treatment yields clinical improvements in

Postby leonardo » Fri Nov 18, 2016 10:03 am

Hi,

In this article they try to explain why 90% of population has EBV but less than 1% has MS:

http://multiple-sclerosis-research.blog ... cells.html

To date, the autoimmune hypothesis around MS is basically attributed to T cells; for instance, crossreactive CD4+ Tcells recognising EBV and myelin epitopes as one and the same (resulting in the proinflammtory targeting of myelin and demyelination). What about B cells? 'tHart et al. argue using evidence from the marmoset model, that B cells infected with the virus may endow them with the capacity to activate self aggressive CD8+ T cells already present in our immune repertoires (normal B cells are less capable of doing this). Moreover, they state that the frequency of human B cells that actually contain the virus is small (<0.01%) , which may explain the low frequency of MS in the population despite the high prevalence of EBV! And, that is how a new hypothesis is born.
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Re: EBV targeting treatment yields clinical improvements in

Postby Leonard » Fri Nov 18, 2016 10:51 am

leonardo wrote:Hi,

In this article they try to explain why 90% of population has EBV but less than 1% has MS:

http://multiple-sclerosis-research.blog ... cells.html

To date, the autoimmune hypothesis around MS is basically attributed to T cells; for instance, crossreactive CD4+ Tcells recognising EBV and myelin epitopes as one and the same (resulting in the proinflammtory targeting of myelin and demyelination). What about B cells? 'tHart et al. argue using evidence from the marmoset model, that B cells infected with the virus may endow them with the capacity to activate self aggressive CD8+ T cells already present in our immune repertoires (normal B cells are less capable of doing this). Moreover, they state that the frequency of human B cells that actually contain the virus is small (<0.01%) , which may explain the low frequency of MS in the population despite the high prevalence of EBV! And, that is how a new hypothesis is born.


Interesting
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Re: EBV targeting treatment yields clinical improvements in

Postby grandsons4 » Fri Nov 18, 2016 12:42 pm

Making no pretense as to understanding the science, I was blown away when I, in an effort to better understand the above article, researched the word "citrullination" in Wikipedia. So many of the subjects discussed at length in these forums appear in the Wikipedia article, and other connections can be drawn by inference (gout/no MS, MS/no gout; smoking and MS). Am I being overly optimistic in thinking that this research is, for lack of a better word, groundbreaking? What do the more scientifically-inclined think?
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