Paraneoplastic Antibodies are caused by tumors which express antigens found only in neural tissue. If you look at the types of cancers that have paraneoplastic several have connections to the epstein-barr virus. This would not be caused by autoimmune cross-targeting.
Epstein-barr (mono) is a herpes virus HHV4 which means it may use estrogen receptors to infect. In nerves it would use the beta estrogen receptor which cycles to the mitochondria and allows it to hide in nerves. In adrenal cells with estrogen receptors it would cycle to the nucleus and could alter gene expression. It would be interesting to test if all non nerve, non beta receptor, estrogen activating cells trigger the immune system differently. Is it changed gene expression or the HHV4 virus.
This is a noticeable correlation not proven.
Thymoma and epstein-barr
http://www.ncbi.nlm.nih.gov/pubmed/2837902
Hodgkin's and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1186979/
Breast carcinoma and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078605/
(For Hodgkin's) the B cells express the estrogen receptor which the EBV uses
http://www.ncbi.nlm.nih.gov/pubmed/12070310
Burkitt's lymphoma is proven to be caused by epstein-barr
Note that the tumors will generate the auto-antibodies but these antibodies should not be able to get into the brain unless a hole in the blood brain barrier exists. Larger infections can make holes: T.gondii, mycobacterias, strep, sutterella....if a hole exists I think gluten sensitivity occurs.
Further note that the oral herpes virus has been found to be inhibited by lysine and encouraged by arginine. There is no evidence to support epstein-barr HHV-4 acts like HHV-1 but one could try.
http://www.ncbi.nlm.nih.gov/pubmed/640102
http://www.ncbi.nlm.nih.gov/pubmed/6262023
No Epstein-barr vaccine is available
http://www.boston.com/news/health/articles/2008/10/06/why_is_there_no_vaccine_against_infectious_mononucleosis/
Epstein-barr (mono) is a herpes virus HHV4 which means it may use estrogen receptors to infect. In nerves it would use the beta estrogen receptor which cycles to the mitochondria and allows it to hide in nerves. In adrenal cells with estrogen receptors it would cycle to the nucleus and could alter gene expression. It would be interesting to test if all non nerve, non beta receptor, estrogen activating cells trigger the immune system differently. Is it changed gene expression or the HHV4 virus.
This is a noticeable correlation not proven.
Thymoma and epstein-barr
http://www.ncbi.nlm.nih.gov/pubmed/2837902
Hodgkin's and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1186979/
Breast carcinoma and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078605/
(For Hodgkin's) the B cells express the estrogen receptor which the EBV uses
http://www.ncbi.nlm.nih.gov/pubmed/12070310
Burkitt's lymphoma is proven to be caused by epstein-barr
Note that the tumors will generate the auto-antibodies but these antibodies should not be able to get into the brain unless a hole in the blood brain barrier exists. Larger infections can make holes: T.gondii, mycobacterias, strep, sutterella....if a hole exists I think gluten sensitivity occurs.
Further note that the oral herpes virus has been found to be inhibited by lysine and encouraged by arginine. There is no evidence to support epstein-barr HHV-4 acts like HHV-1 but one could try.
http://www.ncbi.nlm.nih.gov/pubmed/640102
http://www.ncbi.nlm.nih.gov/pubmed/6262023
No Epstein-barr vaccine is available
http://www.boston.com/news/health/articles/2008/10/06/why_is_there_no_vaccine_against_infectious_mononucleosis/
Autoimmune cross-targeting hypothesis: a virus marks the inside of a cell while a larger infection marks the outside and the combination triggers autoimmune disease. The immune system is instructed to destroy both the inside and the outside of the target.
Do the antibodies entering the brain trigger an autoimmune attack on a part of the brain?
In this case the viral trigger is further away but still marking the target?
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