EBV and low vitamin D possibly work together
Posted: Tue Jun 19, 2007 7:10 am
This new proposal brings together two existing theories about the aetiology of M.S. It suggests that low vitamin D levels at the same time as infection with the Epstein Barr virus could have a detrimental effect on the immune system.
Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis.
Med Hypotheses. 2007 Jun 13;
Authors: Holmøy T
MS risk is associated with low vitamin D status prior to disease, and Epstein Barr virus (EBV) infection seems to be a prerequisite for MS. EBV could activate autoreactive T cells by several mechanisms, but it is not clear why this leads to MS. Only a small proportion of those infected with EBV develops MS, whereas autoreactive T cells are present in the normal T cell repertoire. Genetic factors cannot explain this enigma alone, because the genetic predisposition to MS in most cases is quite weak. Vitamin D receptors are expressed on EBV infected B cells, antigen presenting cells and activated lymphocytes, and the bioactive vitamin D metabolite dihydroxyvitamin D(3) suppresses antibody production and T cell proliferation and skews T cells towards a less detrimental Th2 phenotype. EBV infected B cells constitute a constant challenge to the immune system, also during seasonal periods of relative low vitamin D status. I propose that vitamin D modulates the immune response to EBV, and that detrimental activation of autoreactive T cells leading to MS is more likely if the vitamin D status is suboptimal.
PMID: 17574770 [PubMed - as supplied by publisher]
Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis.
Med Hypotheses. 2007 Jun 13;
Authors: Holmøy T
MS risk is associated with low vitamin D status prior to disease, and Epstein Barr virus (EBV) infection seems to be a prerequisite for MS. EBV could activate autoreactive T cells by several mechanisms, but it is not clear why this leads to MS. Only a small proportion of those infected with EBV develops MS, whereas autoreactive T cells are present in the normal T cell repertoire. Genetic factors cannot explain this enigma alone, because the genetic predisposition to MS in most cases is quite weak. Vitamin D receptors are expressed on EBV infected B cells, antigen presenting cells and activated lymphocytes, and the bioactive vitamin D metabolite dihydroxyvitamin D(3) suppresses antibody production and T cell proliferation and skews T cells towards a less detrimental Th2 phenotype. EBV infected B cells constitute a constant challenge to the immune system, also during seasonal periods of relative low vitamin D status. I propose that vitamin D modulates the immune response to EBV, and that detrimental activation of autoreactive T cells leading to MS is more likely if the vitamin D status is suboptimal.
PMID: 17574770 [PubMed - as supplied by publisher]