This Is MS Multiple Sclerosis Community: Knowledge & Support

High frequency of co-infection by Epstein-Barr virus types 1 and 2 in patients with multiple sclerosis
July 23rd, 2011 by kathibbetson
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authors: Santón A, Cristóbal E, Aparicio M, Royuela A,
Villar LM, Alvarez-Cermeño JC.
source: Mult Scler. 2011 Jul 14. [Epub ahead of print]

A paper was published this month which examines the hypothesis of a causal
link between Epstein-Barr virus (EBV) infection and MS. It compares the frequencies of types 1 and 2 EBV and co-infections in both people with MS and healthy controls.

Eostein Barr Virus
There are two strains of Epstein Barr virus, labelled EBV-1 and EBV-2 (also known as type A and type B). However , although there are some differences, the acute illnesses caused by the 2 strains are apparently identical. Both strains are prevalent throughout the world and can
simultaneously infect the same person. The common names for these infections are Glandular fever or herpes simples ( cold sores and genital herpes)
EBV was detected in 93% of the people with MS and 66% of controls. Interestingly,
dual infection with strains 1 and 2 was seen in 90% of the group with MS but
only 37% of controls (p<0.001) suggesting that co-infection with dual
strains of EBV may be important.
This study provides molecular evidence associating co-infection of type 1
and 2 EBV with MS.

www.med.wisc.edu/news-events/news/drugs ... ases/26288

Could this be a potential drug to kill off latent EBV infections? And would that help pwMS?

interesting find, Cece. I would think that, given all of the evidence associating EBV with MS, more research would certainly be warranted using this drug therapy on MS patients.

It's interesting that this drug destroys cells harboring EBV, which usually takes up residence in immune system B cells in the human body. The drug Rituxan also destroys B cells, and has been shown to be quite effective in reducing relapse rates and enhancing lesions in RRMS patients. I've often wondered if the action of Rituxan might be attributed to its ridding the body of EBV rather than its immunosuppressive properties, as is commonly supposed.

Since the experimental drug referenced in the article you cited also kills cells infected with EBV, it would likely also have an immunosuppressive effect. I'm not sure which other cells EBV hides out in when it goes latent in the human body…

_________________
Marc
www.wheelchairkamikaze.com

a quick research search turned up these:
www.ncbi.nlm.nih.gov/pmc/articles/PMC2879875/
www.pnas.org/content/107/7/3146.short
www.ajcr.us/files/ajcr0000069.pdf
www.ingentaconnect.com/content/ben/cpb/ ... 2/art00009

The focus is using this potential drug for viral-induced cancers, in particular two cancers (EBV-positive lymphoproliferative disease and fulminant mononucleosis) that require the continued presence of EBV. "Geldanamycin analogues are currently in clinical trials for various types of cancers." It's in clinical trials, if geldanamycin analogue is the same as what we're discussing, so it's past the mouse and test tube stages, which is good. Maybe some enterprising MS neurologist might look into this for us.

And the work was supported by a NIH grant. At least, if they're not yet funding CCSVI research, they are funding other excellent research.

Any difference in the prevelance of EBV in RRMS and PPMS patients?

Here's another for you. I'm sure the oxygen-deprived line will set your CCSVI hearts all aflutter.

http://www.ncbi.nlm.nih.gov/pubmed/14579785

Recent data show that geldanamycin can protect the brain against stroke in vivo, and this may be due to induction of heat shock proteins. Our previous results show that heat shock protein 70 expression by retroviral transfection protects astrocytes from necrotic injury by combined oxygen-glucose deprivation, an in vitro model of ischemia. This study tested the ability of geldanamycin to protect astrocytes from either necrotic or apoptotic injury induced by oxygen-glucose deprivation. Astrocytes were pre-treated with 0.1 microgram ml-1 geldanamycin in the medium 4, 8, or 16 h before as well as during oxygen-glucose deprivation. Increased protein levels of heat shock protein 70 were observed after 8 h pre-treatment with geldanamycin and increased further at 16 h pre-treatment, as detected by immunoblotting. Geldanamycin pre-treatment protected mature astrocytes from necrotic cell death and young astrocytes from apoptotic death. Geldanamycin protection of astrocytes against in vitro ischemia is likely due to upregulation of heat shock protein 70.

heart afluttering....

It protects astrocytes from oxygen & glucose deprivation and it kills latent EBV and it may have immunomodulatory effect (by killing B cells where EBV is hiding)?

Geldanamycin! C'mon big pharma, do this one right!

I don't suppose it comes from hamster ovaries or Chinese fungi or that sort of thing? All the best drugs do....

If MS is caused by a virus wouldn't that make it a potentially communicable disease? Should we be cautious about kissing our loved ones?

We are not contagious.
We can donate blood because they said, not one case of MS was ever found in a spouse of a PwMS. Unless, of course, they married a person known to have MS prior to their marriage.
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Late night thinking:

EBV could be why MS is being found more in children, and presents differently. EBV is usually contagious early in childhood and teens.

The EBV virus may be the link that triggers the birth defected veins to get worse over time. This would also depend what defects one has, and how bad their case of EBV is, or how often it is re-activated, like as a relapse would, or progression. Or are our veins just bystander damage?

Some have extreme Mono others just get the sniffles and never know they were exposed. A simple blood test to find out if you were exposed and if it is latent. It makes sense it could trigger many problems when it is re-activated, perhaps by molecular mimicry, like PR and some of the other herpes viruses re-activate. Thus the autoimmunity and inflammation both can play a part in the mystery. B and T cells too. JMO

But not another drug. Unless it is a two week dosage treatment. A Mycin group drug. Or perhaps one quick needle stick to kill the EBV buggers hiding out.

_________________
Where there is a will, there is a way. "HOPE"

CCSVI Procedure December 2010

Hi!

Is not shingles and Chicken Pox not Epstein Barr related?

If so you wont find many that havent had one or the other.

Fiona

Hi Fiona,
Some say some cancers, some researchers say Chronic Fatigue Syndrome are part of the virus. It is best described here:

http://www.nlm.nih.gov/medlineplus/tuto ... 299103.pdf

_________________
Where there is a will, there is a way. "HOPE"

CCSVI Procedure December 2010

Hi!

I cant access files I think because cookies are disabled.

I think that the virus can lay dormant and resurface as fatigue. I posted my theory on here a couple of weeks back.

That why I dont read loads of research etc. as colours your judgement, I just look into possibilities as an independant.

There is too much research on irrelevant stuff, I just dont read any of it, as to me they are all barking up the wrong tree. In my opinion.

Some would call me crazy, but the more I learn the more I doubt the diagnostic process of why lesions occur even.

Fiona

Shingles and Chicken Pox are caused by Varicella Zoster Virus. Both VZV and EBV belong to the group of Human Herpes Viruses, but they're not the same.

Both viruses reach a very high rate of infection in humans, so indeed it's difficult to tell a difference.

What's remarkable --next to the findings of course-- in this study is the rather low rate of EBV found in HCs. Does it really reflect the reality very well when the control group only has 3/4 of the number of infections that you'd normally expect?

It was co-infections of strain 1 and 2 of EBV. Co-infections are found in other diseases, like sjogrens, but not in the healthy controls of this one study. But honestly, there are so many infections implicated in MS, we just end up going round in circles, with nothing concrete....EBV, HHV, other viral and environmental factors. For those on Facebook, I wrote a note on this topic.
https://www.facebook.com/note.php?note_ ... 4070547211
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Well, yes, I noticed. That was the part "90% dual infection in PwMS vs 37% dual infection in HCs" , I believe that's the gist of it and that's a remarkable finding (what I referred to as "findings" above )

What I meant though was the first remark -- 93% EBV in PwMS vs 66% EBV in HCs. And there I do recall rate of infection numbers considerably higher than 66% in the general population.

My question is, if we assume a general rate of infection around 90-95% .. does any control group that does not meet this rate even serve as a proper control group?