yes, and the xylitol they're adding these days can kill your dog! ...not that i'm brushing my dogs teethlyndacarol wrote:CVfactor – switching to baking soda may not be a bad idea. I think the sugar alcohol, sorbitol, in most toothpastes triggers the pancreas to produce extra…… insulin!
To explain this a little more, in the immune system there are antibodies generated (called IgG or immunogobulin) that are developed by B-Cells which becomeWe have identified at least 2 highly promiscuous major histocompatibility complex class II T-cell epitopes in the Fc fragment of IgG that are capable of specifically activating CD4+CD25HiFoxP3+ natural regulatory T cells (nTRegs). Coincubation of these regulatory T-cell epitopes or “Tregitopes” and antigens with peripheral blood mononuclear cells led to a suppression of effector cytokine secretion, reduced proliferation of effector T cells, and caused an increase in cell surface markers associated with TRegs such as FoxP3. In vivo administration of the murine homologue of the Fc region Tregitope resulted in suppression of immune response to a known immunogen. These data suggest that one mechanism for the immunosuppressive activity of IgG, such as with IVIG, may be related to the activity of regulatory T cells. In this model, regulatory T-cell epitopes in IgG activate a subset of nTRegs that tips the resulting immune response toward tolerance rather than immunogenicity.
So, the theory is that you have effector T cells that are cross reactive to self epitopes as well as to the viral antigens. Normally when the virus is cleared, the ratio of viral antibodies to virus increases and the regulatory T-cells would be activated to shut down the immune response. But it seems that in people with MS, there are defects in these regulatory T cells (number or function), so autoimunity would occur.When IgG and antigen (either complexed or separately) are internalized into the same APC (and TLR ligands or other “danger signals” are present), the response to effector epitopes may outnumber the Tregitopes, resulting in an initial inflammatory response. As antigen is cleared and the ratio of Ig to antigen increases, the balance tips toward tolerance, diminishing immune response and reducing further tissue damage and adverse systemic effects.
Further studies need to be performed, but these Tregitopes may provide an explanation for the limited immunogenicity of Fc fusion proteins, the expansion of CD4+CD25Hi regulatory T cells after administration of therapeutic IVIG,8 and the observed effect of immunoglobulin therapy on autoimmune diseases and other medical conditions.
You should try and train them to rinse and spit the mouthwash!shaight wrote:yes, and the xylitol they're adding these days can kill your dog! ...not that i'm brushing my dogs teeth
Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent form in memory B cells in the majority of the world population. Although, primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis, the virus is associated with a wide variety of neoplasms developing in immunosuppressed or immunodeficient individuals, but also in patients with an apparently intact immune system. In memory B cells, tumor cells, and lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the expression of the viral genes is highly restricted. There is no virus production (lytic viral replication associated with the expression of all viral genes) in tight latency. The expression of latent viral oncogenes and RNAs is under a strict epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of latent promoters in tumor cells, germinal center B cells, and LCLs. Both the latent and lytic EBV proteins are potent immunogens and elicit vigorous B- and T-cell responses. In immunosuppressed and immunodeficient patients, or in individuals with a functional defect of EBV-specific T cells, lytic EBV replication is regularly activated and an increased viral load can be detected in the blood. Enhanced lytic replication results in new infection events and EBV-associated transformation events, and seems to be a risk factor both for malignant transformation and the development of autoimmune diseases. One may speculate that an increased load or altered presentation of a limited set of lytic or latent EBV proteins that cross-react with cellular antigens triggers and perpetuates the pathogenic processes that result in multiple sclerosis, systemic lupus erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE patients EBV may cause defects of B-cell tolerance checkpoints because latent membrane protein 1, an EBV-encoded viral oncoprotein can induce BAFF, a B-cell activating factor that rescues self-reactive B cells and induces a lupus-like autoimmune disease in transgenic mice.
Primary Infection with the Epstein-Barr Virus and Risk of Multiple Sclerosis
To determine whether multiple sclerosis (MS) risk increases following primary infection with the Epstein-Barr virus (EBV), we conducted a nested case-control study including 305 individuals who developed MS and 610 matched controls selected among the over 8 million active-duty military personnel with serum stored in the Department of Defense Serum Repository. Time of EBV infection was determined by measuring antibody titers in serial serum samples collected before MS onset among cases, and on matched dates among controls. Ten (3.3%) cases and 32 (5.2%) controls were initially EBV negative. . All of the 10 EBV-negative cases became EBV positive before MS onset ; in contrast, only 35.7 % (10) of the 28 controls with follow-up samples seroconverted (exact p value = 0.0008). We conclude that MS risk is extremely low among individuals not infected with EBV, but it increases sharply in the same individuals following EBV infection.
CD8+ T-cell deficiency is a general feature of chronic autoimmune diseases and also occurs in healthy blood relatives of patients with these diseases. It is proposed that this deficiency is genetically determined and underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of EBV infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells. Autoimmunity is postulated to evolve in a series of steps culminating in the development of ectopic lymphoid follicles containing EBV-infected autoreactive B cells in the target organ. It is also proposed that deprivation of sunlight and vitamin D facilitates the development of autoimmune diseases by aggravating the CD8+ T cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
Another fascinating post, CV. Just my mind wandering. . . . . If EBV does play a significant role in the development of MS (via costimulatory signals), I wonder why anti-viral drugs (such as Acyclovir and Gancyclovir that also work against EBV) don't appear to have any effect on the course of MS. Perhaps just too late like closing the barn door after the horse has left?CVfactor wrote:Here is a new article on the unifying theory of MS:
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis
http://www.hindawi.com/journals/ad/2012/189096/CD8+ T-cell deficiency is a general feature of chronic autoimmune diseases and also occurs in healthy blood relatives of patients with these diseases. It is proposed that this deficiency is genetically determined and underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of EBV infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells. Autoimmunity is postulated to evolve in a series of steps culminating in the development of ectopic lymphoid follicles containing EBV-infected autoreactive B cells in the target organ. It is also proposed that deprivation of sunlight and vitamin D facilitates the development of autoimmune diseases by aggravating the CD8+ T cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
So Im not sure you can eliminate the virus from the body totally, except with HSCT which would only be until you re-acquire the virus. But since you are also erasing the immune system biography your odds of getting MS would seem low to me.November 7, 2011 — An Epstein-Barr virus (EBV)
vaccine in the early phases of development may
prove able to prevent infectious mononucleosis and
EBV-associated cancers, without necessarily
preventing the EBV infection itself. The vaccine
targets the EBV glycoprotein gp350, which is the
most abundant glycoprotein on the virus and on
virus-infected cells.
Hi CV. . . . sorry to hear about your ADEM. May I ask?. . . since ADEM is very similar in symptomatic manifestation to MS, how do you specifically know that its ADEM and not MS? What age were you diagnosed? Seems like ADEM is mostly diagnosed in a younger age bracket as compared to the (mostly) young adulthood (average around 30 years of age) with MS. And with ADEM there clearly is a strong and obvious correlation with a viral load from infections or live vaccinations, EBV being a major suspected culprit. So this also makes sense that there is so much potential similarity with MS. Did your ADEM go into remission, or are you part of the minority in which it became chronic and is still active?CVfactor wrote:George, good question about antiviral drugs but Im not an expert in this area. My guess would be that they prevent manifestations of EBV such as mono but do not eliminate the virus itself.
Here is a article on a EBV vaccine that may be entering phase III trials:
http://www.medscape.com/viewarticle/753031So Im not sure you can eliminate the virus from the body totally, except with HSCT which would only be until you re-acquire the virus. But since you are also erasing the immune system biography your odds of getting MS would seem low to me.November 7, 2011 — An Epstein-Barr virus (EBV)
vaccine in the early phases of development may
prove able to prevent infectious mononucleosis and
EBV-associated cancers, without necessarily
preventing the EBV infection itself. The vaccine
targets the EBV glycoprotein gp350, which is the
most abundant glycoprotein on the virus and on
virus-infected cells.
I think science may be a long way from eliminating EBV from humans, but I think this would most likely prevent people from getting MS.
Personally I think that both EBV and vitamin D have a role. When I first was struck with ADEM I caught a "flu" from my nephew and after a few weeks the world came crashing down on me. I found out in the hospital that my vitamin D level was quite deficient. Maybe it is a coincidence or maybe I was one of those people who were exposed to EBV later in life.
Also my mother had Hoshimotos thyroiditis, so there is definetely something with genetics, environment and temporal exposure that sets this in motion from my point of view.