This Is MS Multiple Sclerosis Knowledge & Support Community

I absolutely agree EBV is central to MS but it is the inability to manage the virus that sets us apart. That is why I wrote "Beyond Avonex and Valtrex" in the regimens section. We have an inherent issue with vasodilation, vitamins A, B12 and D and chronic inflammation that is observed in other diseases as well. When these symptoms already are an issue then susceptibility to EBV is significant. In time, I suspect Penders work will be very highly regarded but it won't turn out to be the whole answer. As I discussed in the post mentioned earlier we can't ignore the malfunction in the kidney/renal axis and just focus on the virus. Both issues need to be addressed.

Regards

[...........

It is hype, but it also ain't a mouse.

Liberation wrote:So, I can't see any sign that their claim of a potential treatment of progressive MS is well founded based on the treatment of one patient who seems to have had active lesions. It is very misleading to draw such a conclusion. Why couldn't they repeat the treatment with a typical progressive patient who have no gadolinum enhancing lesions before making such a hype statement?

This is a good point.

You can say the same thing about the novantrone trials actually

Researchers like to create hype so that they can get funding for future projects. Obviously, a case report is a very low quality of evidence anyways because the results can be biased by the placebo effect/regression to the mean/random chance and so forth

-c

Just found this interesting remedy, "Gene Eden" that claims to remove latent EBV from the body:

http://www.prweb.com/releases/2014/01/prweb11462653.htm

http://www.buy-gene-eden.com/EBV.php

gainsbourg

gainsbourg wrote:Just found this interesting remedy, "Gene Eden" that claims to remove latent EBV from the body:

http://www.prweb.com/releases/2014/01/prweb11462653.htm

http://www.buy-gene-eden.com/EBV.php

gainsbourg

very interesting...

any reports about experiences ?

I have a very very high load of Epstein-Barr antigens; my gut is ok, at least it is not leaking
I am sure the EBV causes my MS.

the webpage also suggests the link with Hepatitis.
this is very remarkable because I was vaccinated for Hepatitis just a few years before the outbreak/diagnosis of my MS and - I guess - the EBV/Herpes/Hepatitis load of antigen....

if this hypothesis is right, the French were right to prohibit Hepatitis vaccination.
in particular for MS and immune disease susceptible people (multi factor issue incl. cell gates = mitochondrial health, EBV suppression by B-cells, ccsvi that inflammates the cartilage of dural sinus etc. etc)

this is really getting unbelievable; it all fits together in a plausible way...

gainsbourg wrote:Just found this interesting remedy, "Gene Eden" that claims to remove latent EBV from the body:

http://www.prweb.com/releases/2014/01/prweb11462653.htm

http://www.buy-gene-eden.com/EBV.php

http://www.buy-gene-eden.com/Q&A.php

What are the Gene-Eden-VIR ingredients?

Gene-Eden includes five natural ingredients: Camellia Sinensis Extract, Quercetin, Licorice Extract, Cinnamomum Extract, and Selenium. The Gene-Eden-VIR formula is patent protected.

It doesn't sound like it's worth $43/bottle.

Licorice can cause pseudo hyperaldosteronism. I'm not sure that would be a good thing for msers as those of us in the inflammatory phase probably have excess aldosterone circulating already.

NHE wrote:It doesn't sound like it's worth $43/bottle.

haha. Indeed!

Reviewing the article which they cite as making the supplement "clinically proven,"

http://www.buy-gene-eden.com/PP_Gene-Ed ... iviral.pdf

...They site absolutely no evidence anti-EBV properties whatsoever and site only vague benefits which should probably be attributed to the placebo effect in an unblinded trial:

"The participants reported no side effects after taking Gene-Eden-VIR. Seventy three percent of the individuals treated withGene-Eden-VIR reported a decrease in their symptoms. Specifically, they reported a
decrease in the severity (p = 0.006,n = 45), duration (p = 0.009, n = 34), and frequency of their symptoms (p < 0.001, n = 31). Following treatment, theparticipants also reported an increase in their physical abilities (p < 0.001, n = 47), energy levels (p < 0.001, n = 54),mental abilities (p < 0.001, n = 44), and general health (p< 0.001, n = 46). "

What a scam.

cinnamon? Selenium? You have got to be kidding me. If they turn a profit, I will lose all confidence in humanity.

Liberation"
Cheer, you made a very good point, I agree with you. Both SPMS and PPMS patients have less and eventually no gadolinium enhancing lesions, so they seem to be without an acute iflammation at a later stage. Gadolinium enhancing lesions decrease over time in both SPMS and PPMS patients to eventually zero. Most PPMS patients have only a short time at the very early stage of the disease when they have active lesions.
So, I can't see any sign that their claim of a potential treatment of progressive MS is well founded based on the treatment of one patient who seems to have had active lesions. It is very misleading to draw such a conclusion. Why couldn't they repeat the treatment with a typical progressive patient who have no gadolinum enhancing lesions before making such a hype statement?
This news seems to be the usual hype of journalists.

In the 7 years I've been following MS research, the hype hasn't really changed--it's meant to get funding.
One thing I noted years ago, was that EBV enters the "lytic", or reactivated phase, in hypoxic situations. We find it reactivated in stroke patients, too.

There has been much made about the connection of the Epstein Barr virus (EBV) and MS. Most people carry the latent, or dormant version of this virus. Nearly 95% of all adults carry the EBV virus.
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.[/b]

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

What might reactivate this virus and cause it to replicate in the B cells?
Why were these cells also in the brains of stroke patients? It's not just about inflammation or the immune system.
Hypoxia. Lack of oxygen reactivates EBV infection. The ischemic injury of slowed blood flow, caused be stroke or CCSVI, could reactivate EBV cells.
EBV in latent infection can be activated to lytic infection by hypoxia treatment.
http://www.journalofclinicalvirology.co ... S1386-6532(06%2900244-7/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC419879/
++++++++++++++++++++++++++++++++++++++++

In fact, researchers have 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

Researchers cannot comment on how cigarette smoking would increase EBV, increase brain atrophy and worsen MS??
Smoking decreases oxygen and increases hypoxia. Hypoxia activates EBV.

still waiting. Dr. Yulin Ge and other members of the ISNVD are now documenting lowered O2 and perfusion in MS brains, and linking it to slowed venous return. And finally, people with MS are being advised not to smoke.
cheer

Estimated to be $6095 for the treatment. It's got a track record too. http://m.bloodjournal.hematologylibrary ... 5/925.full

cheerleader wrote:

Liberation"

Smoking decreases oxygen and increases hypoxia. Hypoxia activates EBV.

cheer

Stress causes frequent breathing and hypoxia so maybe it has some connection with ebv.

The participation of varicella zoster virus in relapses of multiple sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/24635924

OBJECTIVE:
Recent studies have documented the apparent participation of varicella zoster virus (VZV) in the etiopathogenesis of multiple sclerosis (MS). The present study aimed to corroborate the possible presence of VZV during exacerbations of MS.
DESIGN:
Fifty-three patients with definite MS were included; of them, 31 were studied during the first week of a clinical relapse, whereas 16 were studied during remission; 6 patients with progressive MS were also studied. Genes from 5 herpes viruses: varicella zoster, herpes simplex 1 and 2, Epstein-Barr and herpes 6 were studied by polymerase chain reaction in cerebrospinal fluid and in peripheral blood mononuclear cells (PBMC). As controls 21 patients with inflammatory or functional neurological disorders were included.
RESULTS:
DNA from varicella zoster virus was found in the CSF from all MS patients studied during relapse (100%) and in the PBMC from 28 of them (90%). However, VZV DNA was found in the CSF only in 5 MS patients studied during remission (31%) and in the PBMC from 3 of them (19%). VZV DNA was also found, but in lower amounts, in the CSF (83%) and PBMC (33%) from patients with progressive MS. In contrast, VZV was not found either in CSF or in PBMC from controls. Results from the other herpes viruses tested were similar in MS patients and in controls.
CONCLUSIONS:
Our results corroborate the conspicuous, but ephemeral presence of VZV during relapses of MS and support the idea of VZV involvement in the etiopathogenesis of MS. Recent epidemiological and molecular studies as well as reports of severe VZV infections triggered by specifically induced immunosuppression during therapy of MS give additional support to this potential association.

The evidence is mounting that herpes causes MS

I looked at the study about vzv that I posted here and noticed that there were already 4 or 5 same studies, with exactly the same result.

The first one was from 2004.

How long do we have to wait for some conclusions?