Epstein Barr closer to the cause of MS 2 genes found

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.
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PCakes
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Post by PCakes »

I've never understood the EBV connection for the following reason...
Epstein-Barr virus, frequently referred to as EBV, is a member of the herpesvirus family and one of the most common human viruses. The virus occurs worldwide, and most people become infected with EBV sometime during their lives. In the United States, as many as 95% of adults between 35 and 40 years of age have been infected.
http://www.cdc.gov/ncidod/diseases/ebv.htm
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Post by Cece »

Pcakes, same here. Marc posted this the other day though:
www.ncbi.nlm.nih.gov/pubmed/21757537
Mult Scler. 2011 Jul 14. [Epub ahead of print]
High frequency of co-infection by Epstein-Barr virus types 1 and 2 in patients with multiple sclerosis.
Santón A, Cristóbal E, Aparicio M, Royuela A, Villar LM, Alvarez-Cermeño JC.
SourceDepartment of Pathology, Ramón y Cajal University Hospital, IRYCIS, Madrid, Spain.

Abstract
Background: The existence of Epstein-Barr virus (EBV) strains specifically associated with multiple sclerosis (MS) is a matter of controversy. Little is also known about the prevalence of EBV types 1 and 2 in MS patients and the presence of co-infections by both strains. Objective: To make EBV strain type assignment and compare the frequencies of types 1, 2 and co-infections by both in MS patients and healthy controls. Methods: Blood samples from 75 consecutive MS patients and 186 controls were collected. EBV was simultaneously detected and typed using a polymerase chain reaction (PCR) which amplified a strain-specific sequence in the EBV nuclear antigen 2. Results: EBV was detected in 70 out of 75 patients (93.3%) and in 123 of 186 controls (66.1%). Among positive cases, type 1 was found in 6 patients (8.6%) and 40 controls (32.5%), type 2 in 1 patient (1.4%) and 37 controls (30.1%), and dual-infections by both EBV types were detected in 63 patients (90%) and 46 controls (37.4%). Logistic regression models showed that MS was significantly associated with the presence of EBV (p<0.001) and also with dual type infections (p<0.001). Conclusion: This study provides molecular evidence associating co-infection of type 1 and 2 EBV with MS.
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PCakes
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Post by PCakes »

Thanks Cece.. so if you have had both type I and type II would you have had mono twice?.. or am I thinking too simply? (pretty sure that's bad grammar) But then this concept seems simple. :? The EBV question is not new? Is the ability to test and seperate the two strains new?
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Post by cheerleader »

I'm more of the camp that EBV and other viral antibodies exacerbate MS/CCSVI via endothelial dysfunction. Which is why researchers find associations with MS and EBV, Herpes zoster, H-pylori, CpN and other viral and bacterial infectious agents. How can all of these infectious agents be related to MS? Which one is truly causative? It seems to change from week to week, depending on which research paper one reads. Maybe they all contribute via endothelial dysfunction and inflammation.....
OBJECTIVES: The goal of the present study was to determine whether seropositivity to Helicobacter pylori (HP), Chlamydia pneumoniae (CP), and cytomegalovirus (CMV) is associated with systemic inflammation and endothelial dysfunction in healthy male subjects.

BACKGROUND: Chronic infection with certain bacteria and viruses may play an important role in inflammation as the pathogenesis of atherosclerosis.

METHODS: The serum levels of immunoglobulin G antibodies to HP, CP, CMV, high-sensitivity C-reactive protein, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 were determined in 81 healthy Japanese men (40 ± 10 years of age). High-frequency ultrasonographic imaging of the brachial artery was used to study endothelium-dependent (flow-mediated vasodilation) and endothelium-independent (nitroglycerin-induced) vasodilation.

RESULTS: Prevalences of seropositive antibodies to HP, CP, and CMV were 67.9%, 61.7%, and 56.8%, respectively. Infection with HP, CP, or CMV had no relationship with age, blood pressure, or level of serum glucose, lipid, or soluble vascular cell adhesion molecule-1. The levels of C-reactive protein and soluble intercellular adhesion molecule-1 were significantly higher, and flow-mediated vasodilation was significantly lower in subjects with seropositive antibodies to HP than in subjects with seronegative antibodies to HP. Endothelium-independent vasodilation was similar in both groups.

CONCLUSIONS: Chronic infection with HP may be involved in_the development of the atherosclerosis via endothelial dysfunction and systemic and vascular inflammation.
http://content.onlinejacc.org/cgi/conte ... /45/8/1219
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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PCakes
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Post by PCakes »

cheerleader wrote:.. Maybe they all contribute via endothelial dysfunction and inflammation.....
See.. now THAT makes sense!
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Post by Cece »

Yes, that makes sense.

I remember feeling like we had a thousand puzzle pieces of MS. Everything worked a little to help MS or was a minor player in making it worse. Nothing fit together.

CCSVI and the endothelium...the big missing puzzle pieces at the center of the puzzle.... :)
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If CCSVI and EBV ever get linked

Post by milesap »

based on damaging veins you will have the missing mechanism for the cause and effect of MS.
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Post by marcstck »

Just to clear up one point about EBV that often leads to confusion, most people who are infected with the virus never had Mono. Often the infection can show up as a bad cold, or be completely asymptomatic.

To me, the most intriguing theory regarding why the herpes viruses are connected with MS and some other "autoimmune" diseases is that the presence of such "smoldering" infections reactivates normally dormant pieces of ancient retroviral DNA that are resident in the human genome.

Hard as it is to believe, most of the human genome (over 90%) has nothing to do with making humans. Some of it is made up of the remnants of retroviruses that at some point in our evolutionary past were infectious, and in some cases deadly, but eventually simply became part of human DNA.

Retroviruses do their dirty work by inserting their genes into the DNA of the cells they infect, and our evolutionary response to this has been to incorporate them into the human genome, as inactivated genes. Eventually, this is what will probably happen with HIV, after several thousand years.

Anyway, there is growing evidence that in some humans with genetic predisposition, an infection of viruses in the herpes family actually activates some of this ancient viral genes in our own DNA, causing our own cells to express proteins that basically make the immune system go cannibal.

Here's an absolutely fascinating article on this phenomenon, entitled "The Insanity Virus". The title refers to schizophrenia, which also seems to be subject to this phenomenon, but there is much discussion of MS in the article as well…

http://discovermagazine.com/2010/jun/03 ... nity-virus

This is really a must-read…
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Post by bestadmom »

I read it. Interesting stuff. I hope the research studies going on in Switzerland on mice w/ms, are really mice w/ms, not eae.
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milesap
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Review

Post by milesap »

Review the EBV and MS link research at

http://www.msrc.co.uk/index.cfm/fuseact ... pageid/707
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Post by Ernst »

Since I began to read about MS, I have been quite interested about blood-brain-barrier. Many research papers say that disruption of BBB is "hallmark of disease", very key part of MS process. I found this interesting paper, which says that EBV virus "... can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence.."



So bbb in MS-patients is in bad enviroment --> abnormal blood flow & activated viruses --> dysfunction?

http://www.ncbi.nlm.nih.gov/pubmed/20826008

On the other hand.. you could think that reduction with blood flow, would make CNS quite vulnerable target, to opportunistic viruses?
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Post by 1eye »

Just to add my anecdotal subjective $0.02 worth, I had symptoms, including an event that sent me shopping around the neurologists in town, and it went away, and a couple of others, that didn't. Then I had a terrible bad flu where I was in bed for about three weeks and my friend Dr. Bob called me a very sick puppy. Could have been an EBV reinfection: it was in my throat something bad. I started on symmetrel once I was diagnosed, and I have been disabled about 7 years now, and unable to walk without walker. But I haven't had the flu in many years. Now I seldom even get colds, since on symmetrel. Plus I have flu shots every year. And Canada, this glorious nation, I believe still uses mercury in flu shots. So who could tell anything from anything?
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Post by 1eye »

Hard as it is to believe, most of the human genome (over 90%) has nothing to do with making humans. Some of it is made up of the remnants of retroviruses that at some point in our evolutionary past were infectious, and in some cases deadly, but eventually simply became part of human DNA.

Retroviruses do their dirty work by inserting their genes into the DNA of the cells they infect, and our evolutionary response to this has been to incorporate them into the human genome, as inactivated genes. Eventually, this is what will probably happen with HIV, after several thousand years.

Anyway, there is growing evidence that in some humans with genetic predisposition, an infection of viruses in the herpes family actually activates some of this ancient viral genes in our own DNA, causing our own cells to express proteins that basically make the immune system go cannibal.

Here's an absolutely fascinating article on this phenomenon, entitled "The Insanity Virus". The title refers to schizophrenia, which also seems to be subject to this phenomenon, but there is much discussion of MS in the article as well…
That would work well for the species, if we had a mechanism for making viral DNA in our genome inactive (perhaps part of that is how APCs work?) but we need something that works sooner than that, preferably on the individual...
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Post by Amydee01 »

marcstck wrote:Just to clear up one point about EBV that often leads to confusion, most people who are infected with the virus never had Mono. Often the infection can show up as a bad cold, or be completely asymptomatic.

To me, the most intriguing theory regarding why the herpes viruses are connected with MS and some other "autoimmune" diseases is that the presence of such "smoldering" infections reactivates normally dormant pieces of ancient retroviral DNA that are resident in the human genome.

Hard as it is to believe, most of the human genome (over 90%) has nothing to do with making humans. Some of it is made up of the remnants of retroviruses that at some point in our evolutionary past were infectious, and in some cases deadly, but eventually simply became part of human DNA.

Retroviruses do their dirty work by inserting their genes into the DNA of the cells they infect, and our evolutionary response to this has been to incorporate them into the human genome, as inactivated genes. Eventually, this is what will probably happen with HIV, after several thousand years.

Anyway, there is growing evidence that in some humans with genetic predisposition, an infection of viruses in the herpes family actually activates some of this ancient viral genes in our own DNA, causing our own cells to express proteins that basically make the immune system go cannibal.

Here's an absolutely fascinating article on this phenomenon, entitled "The Insanity Virus". The title refers to schizophrenia, which also seems to be subject to this phenomenon, but there is much discussion of MS in the article as well…

http://discovermagazine.com/2010/jun/03 ... nity-virus

This is really a must-read…
Watched an interesting movie, think it was called "Feed Your Brain", about the lack of nutrition in our diet and Dr. Hoffer who treated his schizophrenia patients with niacin and got fabulous results. Wonder if the same could be said of MS patients and niacin, could niacin combat ebv?
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