EBV and HHV6B in MS patients

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EBV and HHV6B in MS patients

Postby dignan » Sun Nov 20, 2005 5:43 pm

Interesting study that again shows a connection between HHV6/EBV and MS. Probably requires further study though, it always does...



Presence of Epstein-Barr virus and human herpesvirus 6B DNA in multiple sclerosis patients: associations with disease activity.

Acta Neurol Scand. 2005 Dec;112(6):395-402.

Hollsberg P, Kusk M, Bech E, Hansen HJ, Jakobsen J, Haahr S.
Institute of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark.

Objective - To assess the presence of Epstein-Barr virus (EBV) and human herpesvirus 6B (HHV-6B) DNA in saliva and plasma from multiple sclerosis (MS) patients enrolled in a randomized, double-blind, placebo-controlled valacyclovir treatment study.

Methods - DNA was prepared following ultracentrifugation of saliva and plasma. EBV and HHV-6B DNAs were determined by real-time polymerase chain reaction.

Results - EBV and HHV-6B DNAs were detected in 41% and 65% of saliva samples, respectively. In patients treated with valacyclovir, the percentage of saliva samples with EBV was significantly reduced (9%; P = 0.000017), whereas the frequency of HHV-6B positive samples was unchanged (57%; P = 0.38). Longitudinal studies demonstrated a time-dependent reduction in the frequency of saliva samples containing EBV following valacyclovir treatment. In contrast, plasma contained EBV and HHV-6B DNAs in 17% and 25% of the samples, respectively, and these numbers were not significantly reduced following valacylovir treatment (13% and 16%, respectively), nor were they different from those of healthy controls (6% and 39%, respectively). Patients with high disease activity had a significantly higher frequency of EBV (P = 0.018) and HHV-6B (P = 0.023) positive samples than did patients with low disease activity. The presence of EBV and HHV-6B was strongly correlated in plasma (P < 0.00000001), but not in saliva (P = 0.41).

Conclusion - MS patients express EBV and HHV-6B in both saliva and plasma, but only the expression of EBV in saliva is significantly reduced following valacyclovir treatment. Although EBV and HHV-6B DNAs can be detected in plasma from healthy individuals, the co-expression of both these viruses in MS patients is highly significant and further associated with clinical activity. The observations of viral DNA in plasma are consistent with an underlying immunologic defect in MS.

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Postby bromley » Mon Nov 21, 2005 5:42 am

Dignan,

The EBV theory has been floating around for years but like most things with this disease they never pin it down - one way or the other.

I think a virus will be identified as the culprit sometime in the future - it would fit with my case as I contracted a bad case of glandular fever when I was 16 (although no MS symptoms until 39). PML (the demyelinating disease which was a feature of the Tysabri fiasco) is known to be caused by the JC virus. Also, I posted some work on bacteria and viruses which the Boston Cure Project had undertaken and EBV was cited as a strong contender. EBV is often caught as a teenager / early 20s so again would fit in with the age at which people are diagnosed with MS. A virus might also explain some of the so called MS outbreaks.

Likewise, I imagine that the EBV virus might be more prevalent in countries further away from the equator - in the same way that some of the diseases experienced around the equator are not experienced further from it.

So one theory could be that if someone contracted EBV (or another virus) at the wrong time in life / or a particular variant of EBV (and that you have a susceptibility) it can trigger MS. I assume that if the virus gets into the CNS that the immune system tries to get rid of it and the cascade of events that we call MS starts.

If this is the case, then I'm not too clear how the current treatments or those being trialled could really help - apart from dampening down the immune response.

A few months ago I came across an article in the UK press about a young girl who had brain tumours which were caused by EBV. Her parents were told that there was no hope but one of the UK Universities had been experimenting with a drug which targetted the virus. Once given this she made a complete recovery. Maybe that will be the answer with MS (he says hopefully)!

But I wish the research funders would take a step back and fund research which delivers an answer e.g in 2006 fund projects focussing on EBV to determine whether it is the trigger or not. If the answer is not, then 2007 should be focussed on another theory. At the moment the research is trying to cover too much and does so too thinly, so too many projects end up with the same phrase 'more research is required'.

My other issues is that although MS is a disease of the CNS, other specialisms should also be involved e.g. virologists, immunologists. I've a niggling fear that neurology researchers are looking at issues which may not be their real area of expertise. A more collaborative approach might produce some better results.

As an aside, I had my appointment with the neurologist at my local hospital to discuss starting a DMD. He was incredibly nice and two trainees sat in on the session.

You really realise how crap this disease is when you are asked questions such as - any cognitive problems / swallowing problems / bladder problems etc etc? Thankfully I could say no to these - stiff knees and a smooth palm on one hand are my only lasting deficits.

He asked whether I had any 'mood' problems - I told him I was always in a bad mood. Why's that he said - when I said because I've got an incurable disease which progressively destroys the CNS, he looked slightly surprised.

In terms of treatment options it came down to the four licenced injectibles - he thought Rebif was as good as any. I also asked about statins and minocycline but he said there was no real trials data on these drugs.

In terms of the future he mentioned Campath and Tysabri. He noted that neuro-protection was the 'holy grail'. So nothing new to note - but this website certainly gives you sufficient up-to-date information to have a sensible discussion with a neuro who specialises in this disease.

He had also received and e-mail from another neuro I had seen at the Institute of Neurology. This was an e-mail which I had sent setting out some of the latest research, some of the key discussions that had taken place on this website, and provided the list of treatments in trial (Dignan's work). He was really impressed and thanked me. I imagine that the list of treatments in trial might find their way into some neurology publication in the future - royalties for Dignan. But one does tend to forget that neuros spend most of their day seeing patients (with a range of diseases) and probably don't have huge amount of time to keep up to speed with the latest research / treatment trials.

The only downside to the appointment was that I was sent for a bloodtest. I was number 121 in the queue (following 120 OAPs). I'll get it done another time!


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Postby bromley » Mon Nov 21, 2005 8:27 am

Me again,

The following gives an overview of EBV which seems to have a hand in a vast range of illnesses including CNS diseases.

http://www.emedicine.com/PED/topic705.htm

The article notes that:

'Neurologic complications are as follows:

Neurologic complications occur in less than 1% of EBV infections and usually develop during the first 2 weeks of EBV infection. In some patients, especially children, the neurologic symptoms are the only clinical manifestation of infectious mononucleosis. Patients often are negative for the heterophile antibody. However, these complications often are severe. Complete recovery is the rule, but fatalities do occur.

Primary EBV infection has been associated with aseptic meningitis, acute viral encephalitis, coma, meningitis, and meningoencephalopathy. Hypoglossal nerve palsy, Bell palsy, hearing loss, brachial plexus neuropathy, and multiple cranial nerve palsies have been described. Guillain-Barré syndrome, autonomic neuropathy, gastrointestinal dysfunction secondary to selective cholinergic dysautonomia, acute cerebellar ataxia, and transverse myelitis have been reported. Metamorphopsia, ie, Alice in Wonderland syndrome, has been described'


If EBV did contribute to MS in some way (the cause or a trigger etc) it might explain why different sufferers experience different disease courses / or why the speed of the disease is different between sufferers. One only has to think of a bout of flu in the office - some sufferers are bedridden for a week, others have a milder experience. Or maybe it's the individual's immune system response that decides the severity of the disease.

It's also quite interesting how many who have RR often experience an attack following a bout of illness such as a virus (my first attack followed a period when I felt feeling really under-the weather etc).


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Postby dignan » Mon Nov 21, 2005 9:42 am

Bromley, glad you had your appointment and that your neurologist wasn't a jackass. One other theory I've heard regarding viruses is that maybe in order for viruses to trigger MS, you need the right genetic makeup, then one must be infected with EBV, and then after the EBV infection, one also gets infected with a second virus, such as HHV6 (I've heard more about HHV6a in connection with MS than about the HHV6b they talk about in this study). Anyway, this theory has some appeal to me because I would hope that if it was as simple as a single virus causing MS they'd have made more progress on figuring it all out by now.
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Postby Jaded » Mon Nov 21, 2005 10:13 am

You guys are such fonts of knowledge.

Thank you both so much. I am learning more by the day.

These boards would not be the same without you! :)

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Postby bromley » Mon Nov 21, 2005 3:04 pm

Here's the article about MS and cancer and killer 'T' cells - it's from the Times newspaper. Although it isn't about MS it shows what EBV can do and a way of tackling it. Might be worth trying the killer T cells on someone with MS to see if there are improvements .



May 21, 2005

'Killer cells' cure girl's brain cancer
By David Lister


A CHILD given days to live has been cured of cancer thanks to an experimental treatment pioneered by scientists at Edinburgh University.
Alex Lowe, of Wigan, 8 at the time, had slipped into a coma and was on the verge of death when her parents begged doctors for an untested treatment. Brain tumours caused by a virus had left her paralysed and struggling to breathe. Her organs were starting to shut down. Chemotherapy had failed.



She had a transfusion of specially selected white blood cells, called “killer T-cells”. It works by targeting a specific cancer-causing virus.

Robert Wynn, a consultant haematologist at Royal Manchester Children’s Hospital who treated Alex, said: “She was essentially dead. She was in a coma and her body showed signs that she was close to death with the tumour.

“What happened was miraculous. She woke up and returned to being a normal girl. I have seen a lot of things in medicine, but I have never seen anything like this.”

Alex, now 10, was given the treatment two years ago. Her recovery has so amazed doctors that the case is featured in this month’s edition of the medical journal Lancet Oncology. She is back at school and now behaves like any other 10-year-old girl, riding her bicycle and playing outside.

Alex’s mother, Lindsay, 33, said that her recovery had been remarkable. Lindsay said: “I was sat at her bedside waiting for her to die. Doctors told us there was nothing more they could do and she might have only a couple of hours left.

“But a friend in the nursing profession came to tell us about the work of scientists at Edinburgh University. She told us there must be something that could be done.” After Alex was given the infusion, which is administered weekly, doctors began to see clear signs that her condition was improving. By the second or third week she was much better.

Until Alex’s recovery the treatment had been used only in patients who had contracted cancers after organ transplants. The case has raised hopes that it can be modified to fight other cancers. Dorothy Crawford, Professor of Medical Microbiology at Edinburgh University, who runs the T-cell “bank” from which the treatment was taken, described the results as dramatic. “If we show it works with this virus then maybe we can grow another bank for another virus,” she said.

After the cell therapy, Alex was given a bone marrow transplant to build up her immune system, which had been virtually wiped out by the virus. A second brain tumour was also successfully destroyed using the treatment and she will now donate bone marrow to her five-year-old brother, Cory, who suffers from the same condition.

Since Alex’s astonishing recovery a further ten patients have been treated with the cell therapy. Doctors now hope to use the treatment to cure other virus-related tumours such as liver and cervical cancer.

Henry Scowcroft, of Cancer Research UK, which has funded the therapy, said that the treatment had been spectacular. He said: “Therapies like this one, which are highly specific but available ‘off-the-shelf’ so that they can be delivered to the patient quickly, have long been a goal of the cancer research community.”

Alex suffered from an immune deficiency that meant her body could not protect itself against the usually harmless Epstein-Barr virus.

Her father, Simon, 35, said last night: “We seem finally to be getting back to the little girl we had before. She’s now full of beans, like any other 10-year-old.

“We’ve been to hell and back, and even deeper if you can imagine that. There’s absolutely no assurance whatsoever that it [Alex’s illness] won’t come back, but since she’s had a bone- marrow transplant she’s got a new immune system so, fingers crossed, that should be it.”
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Postby kareng7 » Mon Nov 21, 2005 3:59 pm

I have a theory about the virus/bacteria connection as well. No proof, just a hunch. My hunch goes something like this. You get infected with EBV and/or HPV and/or HHV6 and/or some other herpes related virus, and/or viruses in general--could also apply to bacteria. Once the virus(es) and/or bacteria enter your system and take up residence in your CNS, and/or your DNA, they can hide and don't show up on the tests docs perform to track them down. Or they mutate and don't show up on these tests. So the standard testing medical professionals use to test for them doesn't work effectively.

Basic biology class says a new generation of human beings occurs approximately once every 25 years, while bacteria, under ideal conditions, are capable of producing a new generation every 20-30 minutes. That's a lot of time to produce mutations/evolutions, including possibly developing ways to integrate so thoroughly into the host that detection is inconsistent and difficult.

http://www.slic2.wsu.edu:82/hurlbert/mi ... Chap4.html
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Postby dignan » Mon Nov 21, 2005 4:07 pm

kareng7, from the little I know, I think your theory seems possible. Different studies using different detection methods come up with different results regarding the presence of viruses in people with MS, so I assume it must be tricky to detect evidence of a virus we might have been infected with years earlier. I just hope they get better at detecting viruses soon and figure out how to cure us.
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Postby SarahLonglands » Mon Nov 21, 2005 4:10 pm

And then we have to realise that viruses are much smaller than bacteria and can easily follow along behind the bacterial infection, and do. Most people given the best testing milieu will show positive for EBV before adulthood. Ditto CPn, the bacteria, and therefore the forerunner. (Although with CPn most places are still using inferior testing methods, so don't show this.)

Sarah :?
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby bromley » Tue Nov 22, 2005 10:15 am

The following is part of an interview which the Boston Cure Porject had with one of Canada's leading MS experts who is looking at MS in children - the extract covers EBV:

Excerpt from interview with Brenda Banwell:

Let s look back a little bit at your previous research. At the Boston
Cure Project we re primarily concerned with finding out what causes MS,
and so we were very interested in the paper you published in JAMA in
April that had some noteworthy results concerning the Epstein-Barr virus
(EBV). Could you recap these findings for us?

This study related to our question of whether or not particular
exposures in the environment, such as viruses, trigger or foster an
abnormal immune response that leads to MS. We looked at the Epstein-Barr virus first because it s a very powerful virus in the human immune
system. It s also ubiquitous, so in Canada 97-98% of the population
ultimately are exposed to it. When we initially proposed to investigate
it, a lot of people wondered how EBV can possibly relate to a disease
like MS when everybody is infected. Our response is that it may not be a
question of whether you get it but when. We hypothesized that if you re
exposed to EBV during a particular window of risk, such as a certain age
range, it may modify how your immune system responds to future events.

What we found is that Canadian children with MS were much more likely to have been exposed to EBV than their age-matched non-MS counterparts. Now if our observation is relevant only in Canada, then you have to ponder what that means. However, if it s relevant across the world despite different geographies and different environments, then our finding has a lot more power. So we ve since expanded our investigation to a six-country study of childhood MS, which is taking place in Canada, the US, Argentina, Finland, Italy, and Russia. We presented our preliminary international data at ECTRIMS, and so far it shows the same results we had in the Canadian data, with 80-85% of children with MS being positive for remote EBV infection, versus somewhere between 25 and 40% of controls.

By the way, one of the world experts on EBV is Dr. Ascherio at the
Harvard School of Public Health, and he and his group of epidemiologists
have been studying EBV in adult MS for a long time.

How might one interpret these results?

Well, they might mean that EBV triggers or is involved in the early
events of MS, or they may just mean that children with MS are more prone to EBV. One step we re taking to help answer this question is including a very detailed panel of about twenty viruses in our prospective Canada study, so when children come in with their first attack, we can see
whether they ve had EBV or other infections. If EBV is there at the
first attack, that supports the idea that it s a trigger; if it comes
between the first attack and second, it may be a propagating agent.

The next step involves designing some assays to look at how T and B
immune cells behave. In other words, although we all get EBV, perhaps
our immune systems handle it differently. If you have been infected with
EBV, the virus will live in your B cells. It remains dormant, but it s
always there. One question is whether there is a difference in the
proportion of infected B cells in people who have MS versus people who
don t. Another question is, do people who have EBV infectivity have a
different immune response? Normally, our T cells monitor the number of
EBV-infected B cells in our bodies, and if there are too many, the T
cells come along and dampen them down. One thing to ask is if you have
MS and you receive your EBV infection when you re young, what happens to your T cells? Obviously they ve proliferated to protect you from EBV,
but in doing that did something about the EBV viral protein trigger those T cells to enter the brain and react? We know that there is at least one region of EBV nuclear protein antigen that has a similar genetic sequence to myelin basic protein (MBP), so could this allow T cells to react against MBP because they previously had to react against EBV? And does this happen at a key vulnerable age when something is happening in myelin maturation or otherwise to allow this abnormal reaction? That s a pretty broad question and there will not be a simple answer, but we re designing some assays to see whether children who have MS react differently to certain antigens compared with children who dont, and then we ll try to see whether that plays a role in how the immune system reacts to actual myelin preparations. There s a great deal of work to take what is currently an observation and move it towards a theory and then towards something more concrete, and we are very much at the beginning. But we have some ideas and we re moving forward.

We know that Epstein-Barr persists in our cells and can be reactivated.
Do you think this reactivation could also be involved in triggering
relapses on an ongoing basis?

That s been postulated as a factor in adult MS. We don t know yet
whether that could be important in kids because we re just starting to
look at that. It s entirely possible that relapses are not due to the
activity of the virus, but rather the reactivation of the immune system.
In anyone who s ever had EBV, periodically during the year, EBV
reactivates and is released from the body which is why it s so
infectious. As that process happens, every time it happens, your immune
system has to respond. So your T cells have to increase in number and
they have to dampen down this proliferating virus again. If your T cells
are more active, one could postulate that that might lead to an
increased chance of there being an MS attack. So it may not be that the
virus itself is in the brain, but just that it triggers your immune
system to activate again, which leads to an increased number of
circulating immune cells, some of which go into the brain and cause yet
another attack. That s very theoretical, but it might be true.

Is anyone working on EBV vaccines to prevent infection, or treatments to
keep it from reactivating, if we should find that EBV is involved in
triggering MS and/or relapses?

Yes, and no. The problem with vaccines for EBV is that you would really
have to understand our biology better to be sure that s the right thing
to do. When you give a vaccine, like the measles-mumps-rubella vaccine,
it s usually designed to instigate immunity against the virus by
creating a circulating set of immune cells that were stimulated against
the vaccine. In other words, you get the immune response without having
a real infection. In MS, it may be not the infection that s the problem
but the ongoing immune response, in which case a vaccine may not be the way to go. My other comment which is more philosophical is that any
virus that has survived to the degree that EBV has, and can exist in
almost every person, suggests that somehow it may confer an as-yet
unrecognized advantage to humans. Rarely in nature does a virus or other infectious organism survive and become ubiquitous in the environment unless the host either gains an advantage from it or is unable to kill it. So before you would want to modify something like that, you would really want to understand what it does. We know for example that EBV inequatorial Africa leads to Burkitt s lymphoma. You might question then why it hasn t been weeded out in humans there. One of the reasons is believed to be that it has some protective effect against malaria. So we need to understand EBV better before we would want to wipe it out, and we also need to understand whether trying to wipe it out might just instigate the disease in everybody. If you gave the vaccine to everybody at the same age, and that age happened to be a bad time for their immune system, we could theoretically make the MS problem worse. Remember that the data we have on EBV is just a highly statistically significant observation. Our responsibility now is to take that observation now and study very carefully its association with the disease to be sure we understand what it means. That s not a simple process, and we re
certainly not suggesting that the virus itself causes the disease. We re
looking at a very complex interaction between the immune system, the
environment, your own genetic predisposition and a little bit of chance.
I don t think any one thing is going to be the final answer, but who
knows? Cervical cancer is now largely known to be an infectious disease
and nobody predicted that 20 years ago.
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Postby dignan » Tue Nov 22, 2005 11:42 am

Thanks for the post Bromley, that is probably the most interesting thing I've ever read about EBV and MS. A lot to think about.
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Postby bromley » Tue Nov 22, 2005 3:48 pm

Dignan,

I've been in correspondence with one of the UK's leading MS experts on this issue. He expressed the following view:

'I believe that MS is due to an infection and that EBV is the most likely candidate at present. This latter is based on a large amount of data that has gradually been accumulating over the years. What we lack is biological plausibility, i.e. how does EBV cause MS. What is important is that inflammation does play a role in MS and targeting inflammation will have positive effects on the disease. In many viral and bacterial infections the superimposed immune response causes the pathology, which may be what is occurring in MS'.

I was also pleased to learn that work was being funded to look at EBV specifically and other work was being undertaken on MS and viruses.

This was good to hear, as I imagine that the drugs companies are putting their research funding into the areas where they will get the best return e.g. drugs which target inflammation / the immune system.

I still have a concern that lots of research is being undertaken but that there is no overarching body to pull the pieces together e.g. a finding from Finnish researchers, a finding from Canadian researchers etc. You only posted something earlier this week on this topic yet between the two of us we have made some links and pulled together recent research / thinking (and we're the ones who are losing grey matter!).

I've alerted the Accelerated Cure Project to the current thread given their interest in identifying a cause/s. Perhaps the Nobel winning scientist who finds that EBV causes or triggers MS might mention Dignan and Bromley in his / her acceptance speech!

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Postby dignan » Tue Nov 22, 2005 7:24 pm

Sarah, I'm glad you mentioned CPn, from everything you and others on this site have written about CPn and MS, I'm a believer that it plays a role, at least for some of us.

Bromley, speaking of the Accelerated Cure project, I was looking at old ThisISMS threads and saw a mention by Art of Alberto Ascherio from Harvard who had done some research on EBV and there is a 2005 study on Pubmed that is the same as all the other stuff we've been posting, but I didn't see it anywhere on this site, so here it is...



2005 May 25;293(20):2496-500.
Comment in: JAMA. 2005 May 25;293(20):2536.

Temporal relationship between elevation of epstein-barr virus antibody titers and initial onset of neurological symptoms in multiple sclerosis.

Levin LI, Munger KL, Rubertone MV, Peck CA, Lennette ET, Spiegelman D, Ascherio A.
Division of Preventive Medicine, Walter Reed Army Institute of Research, Silver Spring, Md, USA.

CONTEXT: Infection with Epstein-Barr virus (EBV) has been associated with an increased risk of multiple sclerosis (MS), but the temporal relationship remains unclear.

OBJECTIVE: To determine whether antibodies to EBV are elevated before the onset of MS.

DESIGN, SETTING, AND PARTICIPANTS: Nested case-control study conducted among more than 3 million US military personnel with blood samples collected between 1988 and 2000 and stored in the Department of Defense Serum Repository. Cases were identified as individuals granted temporary or permanent disability because of MS. For each case (n = 83), 2 controls matched by age, sex, race/ethnicity, and dates of blood sample collection were selected. Serial samples collected before the onset of symptoms were available for 69 matched case-control sets.

MAIN OUTCOME MEASURES: Antibodies including IgA against EBV viral capsid antigen (VCA), and IgG against VCA, nuclear antigens (EBNA complex, EBNA-1, and EBNA-2), diffuse and restricted early antigens, and cytomegalovirus.

RESULTS: The average time between blood collection and MS onset was 4 years (range, <1-11 years). The strongest predictors of MS were serum levels of IgG antibodies to EBNA complex or EBNA-1. Among individuals who developed MS, serum antibody titers to EBNA complex were similar to those of controls before the age of 20 years (geometric mean titers: cases = 245, controls = 265), but 2- to 3-fold higher at age 25 years and older (cases = 684, controls = 282; P<.001). The risk of MS increased with these antibody titers; the relative risk (RR) in persons with EBNA complex titers of at least 1280 compared with those with titers less than 80 was 9.4 (95% confidence interval [CI], 2.5-35.4; P for trend <.001). In longitudinal analyses, a 4-fold increase in anti-EBNA complex or anti-EBNA-1 titers during the follow-up was associated with a 3-fold increase in MS risk (EBNA complex: RR , 3.0; 95% CI, 1.3-6.5; EBNA-1: RR, 3.0; 95% CI, 1.2-7.3). No association was found between cytomegalovirus antibodies and MS.

CONCLUSION: These results suggest an age-dependent relationship between EBV infection and development of MS.

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Postby bromley » Wed Nov 23, 2005 3:09 am

Dignan,

The ACP told me that 'the HHV-6 Foundation is organizing an HHV-6
meeting for this coming April and one of the sessions will focus on MS.
They are also trying to obtain funding for a follow-on workshop which
would discuss MS and pathogens more generally'.

So it looks like viruses are definitely back on the agenda. Hopefully, something will come of the current focus. By co-incidence, I saw an article on HIV / AIDS and the HIV virus can cause damage to the CNS of some sufferers (which shows what viruses can do). I don't know much about HIV / AIDS but the treatment given is called antiretrovirals. If a virus was identified as being the cause / trigger for MS, perhaps these sorts of treatments might be beneficial. Although if EBV is just the trigger to the cascade of events (inflammation, neuro-degeneration etc), then the treatments in the pipeline might be our best bet.

It was good to hear (from the MS expert) that targeting inflammation should have a postive effect on this disease, so I'll start my Rebif in due course.

Sarah, like Dignan said, CPn could also be part of this mess. The CNS seems to be riddled with viruses and bacteria that for whatever reason can cause havoc for those with a susceptibility.

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