Researchers find further evidence linking Epstein-Barr virus

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby dignan » Sat Mar 13, 2010 3:51 pm

I wish they could nail down the role of EBV once and for all...


Absence of Epstein-Barr virus in the brain and CSF of patients with multiple sclerosis.

Neurology. 2010 Mar 10. [Epub ahead of print]
Sargsyan SA, Shearer AJ, Ritchie AM, Burgoon MP, Anderson S, Hemmer B, Stadelmann C, Gattenlöhner S, Owens GP, Gilden D, Bennett JL.
From the Departments of Neurology (S.A.S., A.J.S., A.M.R., M.P.B., S.A., G.P.O., D.G., J.L.B.), Microbiology (D.G.), and Ophthalmology (J.L.B.), University of Colorado Denver School of Medicine, Aurora; Department of Neurology (B.H.), Technische Universität, Munich; Universitätsmedizin der Georg-August-Universität Göttingen (C.S.), Göttingen; and Department of Pathology (S.G.), Julius-Maximilians-University, Würzburg, Germany.

OBJECTIVE: Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that becomes latent in B-lymphocytes and has been implicated in the pathogenesis of multiple sclerosis (MS). We searched for latent and active EBV infection in MS brain and CSF.

METHODS: Nested and non-nested real-time PCR were used to detect cell-specific and EBV-specific transcripts in 15 fresh-frozen and 5 formalin-fixed paraffin-embedded MS plaques and in single MS CSF B-lymphocytes and plasma cells. Intrathecal anti-EBV antibody synthesis was measured by ELISA. Immunocytochemistry was used to detect binding of MS CSF and recombinant antibodies (rAbs) generated from clonally expanded plasma cells in MS CSF to EBV-infected cells.

RESULTS: No EBV RNA was found in MS CSF B-lymphocytes or plasma cells. In active MS plaques, EBV-encoded RNA (EBER)-1 was the only and rarely detected transcript. The frequency of detected intrathecal anti-EBV antibody synthesis in patients with MS did not differ from that in non-MS inflammatory CNS disease control patients. Anti-EBV antibodies were detected in the CSF of patients with MS, but MS rAbs did not react with EBV.

CONCLUSIONS: Application of real-time PCR to multiple sclerosis brain and single B-lymphocytes in CSF did not reveal any evidence of active Epstein-Barr virus infection.

http://www.ncbi.nlm.nih.gov/pubmed/20220124
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Postby gainsbourg » Sat Mar 13, 2010 5:00 pm

Actually, those findings don't surprise me because I believe the researchers are looking up the wrong tree. They are making the assumption that they need to find evidence of herpes attack .... but maybe there isn't any attack even though we know that herpes antibodies are produced in MS.

In war, an invading army doesn't necessarily need to fire a single shot in order to provoke a massive defensive bombardment - purely because it is considered to be a threat. That's what is maybe happening in MS, the presence of herpes hiding and cloaking itself deep in nerve tissue (in one shape or another) is enough to trigger a defensive response. This is mistaken as being the body attacking itself, in other words what seems to be an autoimmune response.

The Sargsyan study confirmed previous findings that herpes antibodies are there:

Anti-EBV antibodies were detected in the CSF of patients with MS


This latest research ignores the fact that herpes antibodies are not found in the CSF of those without MS, or the fact that herpes antibodies (VZV at least) are known to increase in the CSF during MS attacks. Discoveries about herpes have been coming in thick and fast in the last few years. Locating it and understanding it seems to be as complicated as HIV. New discoveries are being made all the time - so don't rule it out just yet!



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Postby catfreak » Sat Mar 13, 2010 5:58 pm

I did not have chicken pox until I was 24, after my 2 children had them. Then at 40 was diagnosed with Mono/EBV at 40. I have had fever blisters as long as I can remember. All of these seemed to have come along as a result of stress.

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Postby rainer » Sat Mar 13, 2010 6:12 pm

I agree with that study being very small (you could prove anything with 15 patients) with a pretty narrow scope.

It'd be nice if they found active EBV in active lesions but I don't think anyone is under the illusion that the relationship would be so simple.

My 2 cents: the latent/active factor needs to be thrown out. It complicates the relationship question and is overvalued b/c of the old myth that latent disease is harmless. This is not true in EBV or MS.
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Re: Researchers find further evidence linking Epstein-Barr v

Postby Anonymoose » Sun Jun 30, 2013 7:23 pm

Wonderfulworld wrote:
VZV vaccine had already been manufactured. I remember that it's only effective for a dozen years or so. Too late to search and see if it's only effective before infection or not, it's way past my bedtime.




Let us know if you find anything L....even a dozen years might buy us a bit of time!



If anyone else can locate info on a substance that interferes with EBV let us know too.



Background: in 1992 or 1993 I was 2 years post-EBV and still feeling ill, but was working on a job and a colleague bought the Irish Times everyday. I remember reading an article that described a herb that blocked EBV (or Glandular Fever) in the blood. Try as I might, I can't find that article, even though the Irish Times archive is digitised here: http://www.irishtimes.com/search/archive.html odd but then again my research skills are not as sharp as they once were.
rainer wrote:A lot of EBV research that I have found points to the development of HSP-90 inhibitors mainly in relation to cancer.



http://en.wikipedia.org/wiki/Hsp90



There is a chart nearly at the bottom this page (http://www.gistsupport.org/ask-the-professional/hsp90-inhibitors-and-gist.php) with many of these inhibitors currently in trials.



Here is an abstract for one recent study relating HSP-90 inhibitors and MS. http://www.ncbi.nlm.nih.gov/pubmed/19948165


Curcumin is a hsp90 inhibitor effective against ebv to some extent...see gibbledeegooks anti-viral thread.
http://www.labome.org/grant/r01/ca/iden ... 36644.html
Identification of Natural Product Inhibitors of Hsp90 as Chemotherapeutic Agents
Summary
Principal Investigator: Robert Matts
Affiliation: Oklahoma State University
Country: USA
Abstract: Hsp90 is widely appreciated for its obligatory role in facilitating protein folding. Of the known Hsp90- dependent clients, 48 are directly related to oncogenesis, with Hsp90 clients being represented in all six hallmarks of cancer. Thus, inhibitors of Hsp90 provide a combinatorial attack that simultaneously derail multiple signaling cascades. Consequently, Hsp90 has emerged as an exciting new target for the development of anti-tumor agents. We have recently discovered that curcumin, a natural product found in Indian curry, inhibits Hsp90. In contrast to geldanamycin-derivatives that are currently in clinical trials, curcumin and its analogues can be easily synthesized for elucidation of structure-activity relationships and enhanced affinity for Hsp90. In addition, several other natural products that affect signaling pathways containing Hsp90-dependent proteins have been proposed to manifest their inhibitory activities through Hsp90 inhibition. Therefore, our specific aims are: 1) to identify new natural product inhibitors of Hsp90, libraries of natural products and their derivatives will be screened for their ability to inhibit the Hsp90- dependent refolding of luciferase and Hsp90's ATPase activity using assays developed in our laboratories; 2) to elucidate the biochemical mechanism of action of identified inhibitors by the use of in vitro assays that clearly differentiate whether molecules bind to Hsp90's N- or C-terminal ATP binding pocket (assays for Hsp90-dependent client maturation, pull down assays to determine effects on Hsp90/co-chaperone/client interactions, and protease fingerprints); 3) to determine the pharmacological properties of inhibitors in cancer cell lines by evaluation in anti-proliferative/ cytotoxicity assays, induction of Hsp90-dependent client protein degradation, and increased Hsp90 levels as hallmarks of Hsp90 inhibition; and 4) to elucidate structure-activity relationships for these inhibitors. Results from this work will identify new natural product inhibitors of Hsp90 and will provide more efficacious drugs that can be easily modified for increased potency against a wide range of cancers, and may lead to the development of more potent and less toxic chemotherapeutic agents. This proposal is innovative because for the first time, we will clearly show that the mechanism of action for natural products (e.g., curcumin) that are currently in clinical trials for the treatment of cancer act through Hsp90 inhibition.
Funding Period: 2009-09-30 - 2011-09-29
more information: NIH RePORT
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Re: Researchers find further evidence linking Epstein-Barr v

Postby cheerleader » Sun Jun 30, 2013 8:12 pm

This thread is from 2010...there's been more on EBV since then.
A recent post mortem study showed reactivated EBV cells in active MS lesions.
In the seven MS patients' postmortem brain tissue studied, active MS lesions all contained Epstein-Barr virus infected cells.

Such cells weren't unique to MS, but were also detected in CNS tissue from two control patients with stroke, which the researchers pointed out is also a disease in which inflammation plays an important role.

Notably, Epstein-Barr virus-positive cells were present in much higher numbers in active MS lesions than expected in peripheral blood B cells, "which suggests that these cells are recruited to or accumulate in CNS infiltrates," Lünemann noted.

http://www.everydayhealth.com/multiple- ... in-ms.aspx

What might reactivate this virus and cause it to replicate in the B cells--in the CNS?
Why were these cells also in the brains of stroke patients?
Hypoxia. Lack of oxygen reactivates EBV infection. The ischemic injury of slowed blood flow, caused be stroke or CCSVI, could reactivate EBV cells.
http://www.journalofclinicalvirology.co ... 86-6532(06)00244-7/abstract
http://www.ncbi.nlm.nih.gov/pubmed/16931136

In fact, researchers have also found a link between pwMS who smoke, and the levels of EBV antigens, or ENBA titers.

The investigators found that among patients with MS, anti-EBNA titers were much higher among smokers than among nonsmokers. In addition, the increased risk of MS associated with anti-EBNA was stronger among those who had ever smoked (odds ratio [OR], 3.9; 95% confidence interval [CI], 2.7 – 5.7) compared with never smokers (OR, 1.8; 95% CI, 1.4 – 2.3; P value for interaction = .001).

By contrast, the association between smoking and MS was not present in individuals with low anti-EBNA titer levels. In addition, the risk of MS associated with smoking did not appear to be modified by HLA-DR15 gene status.

To my knowledge, there is not a well-described causative mechanism linking smoking and MS,” she said. “Possible mechanisms, such as neurotoxicity and immunomodulatory effects, have been suggested, but there is limited data on this topic.”

Asked for comment on these findings, Lily Jung, MD, with the Swedish Neuroscience Institute, in Seattle, Washington, added that recent studies show that not only does smoking increase risk of developing MS, it also increases magnetic resonance imaging lesion volume and brain atrophy and leads to faster progression of the disease.

http://www.medscape.com/viewarticle/720000
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875934/

one explanation---smoking is a known cause of cerebral hypoxia. Hypoxia reactivates latent EBV. Hypoxia is part of MS.
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Re: Researchers find further evidence linking Epstein-Barr v

Postby gainsbourg » Mon Jul 01, 2013 5:18 am

That 2012 study Cheerleader just quoted was the turning point for me.

http://www.everydayhealth.com/multiple- ... in-ms.aspx

From that day on I have been completely certain herpes is the primary cause of MS (EBV is just one of several strains of herpes with a strong association with MS). I had being guessing for years that the mere presence of the herpes virus in nerve ganglia must somehow scare or trick the immune system into action, and this study backed up that hypothesis.

Until that study, almost all researchers had been saying "there's no evidence that herpes attacks myelin" - but since then, we've known for sure that it doesn't have to actually ATTACK. It somehow stimulates the immune system into a needless attack on healthy tissue.

For me it also explains the mystery of the stress/MS relapse relationship. Stress, in its many forms, often precedes herpes attacks. The white matter of the brain and CNS is like a telephone exchange conveying information from one part to another - stress logically puts an extra strain on this amazing system. Living creatures are very much like machines in some respects - certain types of strain or stress can eventually cause problems and damage.

Stress also calls into play huge changes inthe vascular system. Herpes viruses like EBV lie dormant in the base ganglia of the nerves - waiting for some kind of trigger or imbalance.

I am glad Cheerleader bumped this topic and believe that the day we learn how to eradicate herpes - through whatever means - will signal the end of MS



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Re: Researchers find further evidence linking Epstein-Barr v

Postby Anonymoose » Mon Jul 01, 2013 5:31 am

gainsbourg wrote:That 2012 study Cheerleader just quoted was the turning point for me.

http://www.everydayhealth.com/multiple- ... in-ms.aspx

From that day on I have been completely certain herpes is the primary cause of MS (EBV is just one of several strains of herpes with a strong association with MS). I had being guessing for years that the mere presence of the herpes virus in nerve ganglia must somehow scare or trick the immune system into action, and this study backed up that hypothesis.

Until that study, almost all researchers had been saying "there's no evidence that herpes attacks myelin" - but since then, we've known for sure that it doesn't have to actually ATTACK. It somehow stimulates the immune system into a needless attack on healthy tissue.

For me it also explains the mystery of the stress/MS relapse relationship. Stress, in its many forms, often precedes herpes attacks. The white matter of the brain and CNS is like a telephone exchange conveying information from one part to another - stress logically puts an extra strain on this amazing system. Living creatures are very much like machines in some respects - certain types of strain or stress can eventually cause problems and damage.

Stress also calls into play huge changes inthe vascular system. Herpes viruses like EBV lie dormant in the base ganglia of the nerves - waiting for some kind of trigger or imbalance.

I am glad Cheerleader bumped this topic and believe that the day we learn how to eradicate herpes - through whatever means - will signal the end of MS



gainsbourg


I'm starting to lean that way too. I wonder if the immunosuppressives aren't allowing the ebv to spread in the background (hence my link to curcumin as a hsp90 and ebv inhibitor in post before cheer's). Have you found anything to address the ebv issue? I'm about to start digging into rituxan...
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Re: Researchers find further evidence linking Epstein-Barr v

Postby cheerleader » Mon Jul 01, 2013 9:34 am

But EBV was present in the brains of those who had strokes. They did not have MS....there was a break in the blood brain barrier, hypoxia/ischemia, and a reactivation of the EBV virus to the lytic phase in the CNS (EBV is present and latent in 95% of us)----please don't miss the larger point. EBV is reactivated by hypoxia. If we can stop/prevent hypoxic injury to the CNS, EBV may not reactivate.

BNAC explains it this way-

The association between EBV infection and CCSVI has not yet been explored; however, it could be hypothesized that venous stasis in the superior saggital sinus due to extracranial outflow impairment could affect the drainage of bridging veins that pass through the subarachnoid space (near the meninges and EBV-infected B-cell follicles) and contribute to EBV activation. The venous stasis hypothesis in the SSS may contribute to understanding why so many different viruses and bacteria [3,111] have been linked to increased MS susceptibility risk over the last 50 years.

http://www.expert-reviews.com/doi/abs/1 ... ern.11.117

Focusing on one particular virus or bacteria (cpn, borrelia, EBV) may not be the answer. Understanding why these germs reactivate in an MS or ischemic brain, and preventing this situation, may be the answer. You can give immune modulating medications to someone after they have a stroke (since the immune system becomes reactive after a break in the BBB)---but doctors do not recommend this.

"To date, there has been little interest in exploring the possibility that autoimmune responses to brain antigens might affect outcome from stroke. There are, however, studies that document the fact immune responses to brain antigens do occur following stroke.
For instance, lymphocytes from stroke survivors show more activity against MBP than the lymphocytes from patients with multiple sclerosis.

In summary, the nature of the postischemic immune response affects outcome from stroke (Figure). Modulation of this response may be a viable approach to improving outcome in stroke, but there are potential dangers associated with immunomodulation. A more complete understanding of the endogenous immune response following stroke is needed to safely manipulate this response in the poststroke period.

http://stroke.ahajournals.org/content/4 ... 1/S75.full

Instead, stroke prevention, lifestyle modifications (diet and exercise), potential angioplasty/surgery and rehabilitation are recommended.
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Re: Researchers find further evidence linking Epstein-Barr v

Postby Anonymoose » Mon Jul 01, 2013 10:17 am

Maybe the difference between stroke patients and MS patients is the genetic factor. I agree that maximizing overall health is definitely beneficial to MSers but I don't think CCSVI/hypoxia is the cause for everyone. This may be shown in the lack of response in some who pursue CCSVI PTA and see no improvements or those who have only temporary improvements with no restenosis (heavier ebv load?). Surely not all of their procedures failed to reintroduce adequate blood/csf flow. Also, MS exacerbations, in many cases, coincide with increases in ebv load. With CCSVI and chronic hypoxia, one would think the exacerbations would occur more frequently because ebv is allowed to increase at a faster rate...maybe this is the case. If ebv is the ultimate culprit though, it doesn't look like CCSVI PTA will provide long term benefit. CCSVIers will just experience a milder disease progression than they previously had. Are there any studies on cytokine profiles before and after CCSVI? That would be interesting...

The next step for me is rituxan (maybe while on feno...there is a current study using rituxan and copaxone simultaneously. I assume this is to avoid cytokine overload/exacerbation from ebv/b cell die off) and whatever I can do to keep ebv load low (I hope curcumin makes its way to b cells). Rituxan infusion knocks out more than 90% of b cells/ebv hosts so it seems if you keep the remaining ebv from spreading to new b cells and find a way to protect yourself from re-infection, you would experience long term remission from just a few infusions.

Hopefully my neurologist will make it easy for me to get the rituxan infusions. :)
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Re: Researchers find further evidence linking Epstein-Barr v

Postby jimmylegs » Mon Jul 01, 2013 12:03 pm

susceptibility to viral infection (1), risk of venous insufficiency (2), severity of cerebral ischemia (3), stress (4), relapse dynamics (5), smoking (6), and inflammation (7), all have a strong zinc connection in the literature. we can even draw connections to heat shock proteins (hsp) via research on zinc status correlations to membrane integrity in plants (wheat) under heat stress (8). not to mention congenital malformations (9). zinc is arguably a significant piece of the puzzle.

i'm just citing single studies illustrating each point. note the low normal to deficient numbers where highlighted. the actual body of research on many of these items runs far more broadly and deeply than represented here

1. Relationship of Serum Copper and Zinc Levels to HIV-1 Seropositivity and Progression to AIDS (1991)
http://journals.lww.com/jaids/Abstract/ ... _to.9.aspx
"...serum zinc levels were lower (p = 0.016) in the seropositive progressors (mean = 85.2 [mu]g/dl; SD = 11.5) than the seropositive nonprogressors (mean = 90.7 [mu]/dl; SD = 12.0) and the seronegatives (mean = 92.0 [mu]g/dl; SD = 14.7)." [nb normal range for zinc goes down to 75. healthy controls should be up around 120. if I were HIV positive and was being told I was 'normal' at 85 and then found this study, i'd be pissed right off]

2. Effects of long-continued ingestion of zinc sulphate in patients with venous leg ulceration (1970)
http://www.sciencedirect.com/science/ar ... 3670920660
"The mean plasma-zinc concentration in this group was significantly lower before treatment than in a group of control subjects."
[they had good results in the first study but then had trouble replicating the use of zinc for healing over time - they used inorganic zinc sulfate which is inferior to organic forms in terms of bioavailability, esp in conjunction w dietary phytate]

3. Clinical Significance of Serum Zinc Levels in Cerebral Ischemia (2010)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042622/
"Overall, out of the 224 patients analyzed (mean age 67 years), 35.7% patients had low zinc levels (65mcg/dL). Patients with stroke (n = 152) were more likely to have low zinc levels (OR = 2.62, CI 1.92–3.57, P < .003) compared to patients with TIA (n = 72) [transient ischemic attack ie mini-stroke].

4. Decreased Zinc and Increased copper in Individuals with Anxiety
http://www.la-press.com/decreased-zinc- ... icle-a2460
"Mean Zn anxiety 74.47
Mean Zn controls 87.69"

5. have to do a two-step for this one.. i) uric acid varies in ms relapse and remission. ii) zinc intakes and uric acid levels are correlated - in controls as well as subjects so never mind the OCA part
i) Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood–brain barrier dysfunction
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
"MS patients were found to have significantly lower serum uric acid levels (193.89 ± 49.05 μmol/l; mean value ±SD) in comparison with healthy donors (292.7 ± 58.65 μmol/l; P=0.000) and OIND patients (242.7 ± 46.66 μmol/l; P=0.001). We found that MS patients with relapse had significantly lower serum uric acid levels (161.49 ± 23.61 μmol/l) than MS patients with remission (234.39 ± 41.96 μmol/l; P=0.000) and more over, MS patients with BBB disruption had significantly lower serum uric acid levels (163.95 ± 26.07 μmol/l) than those with normal BBB (252.48 ± 25.94 μmol/l; P=0.000). Further, we also found that serum uric acid level independently correlated with disease activity, BBB disruption, and gender."
ii) Effect of low zinc intake and oral contraceptive agents on nitrogen utilization and clinical findings in young women
http://jn.nutrition.org/content/107/12/2219.full.pdf
"Use of contraceptive drugs appeared to influence the response of blood parameters to zinc depletion. ... Serum uric acid ... changed significantly in both groups [with or without OCA]."

taking a break, will be back for 6 through 9 :) ...

the takeaway point is, reduce your risk of all of the above by keeping your zinc levels up near the top of the normal range ie 18.5umol/L or 120ug/dL
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Re: Researchers find further evidence linking Epstein-Barr v

Postby Leonard » Mon Jul 01, 2013 12:59 pm

I think the EBV virus, just like the Clamidia Pneumonia bacteria, has the possibility to block receptors of cells. There are studies that prove this.

When receptors are blocked, the cells are not well fed; they can't sense the insulin anymore, or the leptin. If cells are not well fed, the mitochondria do not work. And if enough of these mitochondria in a cell do not work, the equilibrium of the ion pump can not be maintained. And you get a relapse.

The typical time constant is relatively short, you are in remittance relatively quickly i.e. when the immune system reacts or when you get medication. I think the phenomenon does not point to biological changes (because they would have longer time-constants) but to other processes just like the one I just described with the ion pump.

You then get to the theory behind the new concept for MS.. on that thread you find the links to the studies that found that EBV may block nuclear receptors of the cells...
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Re: Researchers find further evidence linking Epstein-Barr v

Postby orion98665 » Mon Jul 01, 2013 5:36 pm

Very interesting subject... i came across these two articles linking EBV to infecting endothelial cells of BBB

Intriguingly, EBV has been shown in vitro to infect human endothelial cells of the BBB, leading to increased production of chemokines and adhesion molecules. This upregulation of proinflammatory mediators supports increased adhesion of immune cells on the surface of an EBV-infected brain endothelial monolayer.

http://www.medscape.com/viewarticle/780170_5


And this article...

Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis.

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


So my question is, if EBV causes pro- inflammatory mediators or damage to endothelial cells could it be that CCSVI is an effect of MS and not the cause..??


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Re: Researchers find further evidence linking Epstein-Barr v

Postby gainsbourg » Tue Jul 02, 2013 1:58 am

Absolutely. Vascular problems are clearly a frequent symptom of MS - but not the cause. That doesn't mean that treating MS symptoms is a bad thing. As I've often pointed out on this forum, CCSVI is far too common in healthy people to be the cause of MS. Some studies claim it is a common as being lefthanded.

So much evidence now points to herpes as the primary cause of MS. It's interesting to talk about Epstein Barr in isolation, but that's like discussing one strain of influenza instead of the virus as a whole.

The comment below appeared in a forum dedicated to the HHV6 herpes virus. It's a pithy meta-analysis of much of the herpes/MS picture. Worth wading through.

The evidence continues to mount that herpesviruses HHV-6A, EBV and VZV play an important role in triggering multiple sclerosis, perhaps in different subsets. Researchers at Oregon National Primate Research Center recently isolated a gamma herpesvirus that caused symptoms identical to MS in macaque monkeys. Alberto Ascherio at Harvard has shown that elevated EBV EBNA-1 antibodies are a marker for increased risk of MS, and researchers in Mexico recently found that VZV DNA is found in the CSF of 65% of MS patients with the progressive form and Chinese investigators found an increased incidence of MS the year after a VZV shingles attack.

The evidence for HHV-6A seems strongest of all the viruses implicated, although these viruses potentiate each other and co-infections and interaction with endogenous retroviruses appear to play a role as well. Over the past five years, European researchers have shown that HHV-6A can be isolated from the serum and CSF in a subset of MS patients during relapse, and have linked HHV-6A reactivation to two genes associated with an increased risk for MS: IRF5 and MHC2TA rs4774C.

Steve Jacobson at NINDS has shown that there is an increased lymphoproliferative response to HHV-6 and that there are HHV-6 and EBV specific oligoclonal bands in MS patients. Finally, the Spanish investigators also demonstrated that the effectiveness of interferon beta 1b treatment in MS patients correlates with HHV-6 DNA levels, suggesting that it is the antiviral action of the interferon beta treatment that causes the therapeutic effect. Jacobson’s group presented evidence at the last HHV-6 conference last winter that HHV-6A can cause MS-like neurological disease in monkeys (unpublished), and a group from France demonstrated that HHV-6A can cause mice to develop lesions in the brain.

Where is the MS community and why aren’t patients demanding clinical trials with antivirals? Clinicians at NYU tried valacyclovir (Valtrex) in 2005, but this was the wrong drug. Valtrex (which converts to acyclovir) is not effective for HHV-6. The rationale for a trial of valganciclovir (Valcyte) is compelling. It crosses the blood brain barrier, has a relatively good safety profile, and is effective against HHV-6A. FDA approved for CMV retinitis, Valcyte is an oral drug that can be used safely as long as patients are monitored for bone marrow suppression. It has been used routinely as prophylaxis for herpesvirus reactivation in the transplant community for over ten years, with minimal adverse side effects.

The HHV-6A may only be a bystander, and it may be that abortive infection (not actual replication) is what is important in triggering MS. That doesn’t mean an HHV-6 and EBV specific antivirals shouldn’t be given a try – especially in those with signs of viral activity (elevated IgG titers or virus specific oligoclonal bands). It is pretty clear now that interferon works for MS because of the antiviral effect, but it is a relatively weak antiviral compared to the others used for viral reactivation in transplant patients. What are neurologists waiting for?


http://hhv-6foundation.org/community-op ... ical-trial


As the guy says - what are neurologists waiting for? And why isn't there more discussion about natural anti-herpes remedies?

As I said in an earlier post, everyone used to dismiss all the research saying "there's no evidence that herpes viruses actually attack nerve cells", but the 2012 study at Queen Mary University in London showed that they don't have to:

http://www.everydayhealth.com/multiple-

The mere presence of herpes somehow provokes the immune system into attacking healthy tissue.

Venom of various kinds has often been reported as an MS cure (bee; scorpion; jellyfish etc.) Could this be because venom is often anti-viral? I once read that the only substance in the world thought to completely destroy the herpes virus is cobra venom.

Also consider the epidemiology - well known world MS hotspots. Herpes virus outbreaks may be contained in island populations. Could this explain the MS hotspots of Sardinia and The Orkney Islands? Does anyone know if the various herpes viruses, EBV, VZV and hhV-6 are less common in equatorial regions and the far East?




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Re: Researchers find further evidence linking Epstein-Barr v

Postby jimmylegs » Tue Jul 02, 2013 4:24 am

perhaps it's about a fundamental vulnerability to infection by various things .. EBV, HHV, C.pneumonia, candida, etc.
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