Viruses such as Epstein Barr, cause stress to the CNS, which then activates mMC that begin an unending inflammatory cascade resulting in activation of Th-17 pathogenic lymphocytes, oxidative stress, oligodendrocyte cessation, and recruitment of B-cell plasma.
Also, sometimes herpes virus may be involved.
https://www.eurekalert.org/pub_releases/2017-07/uorm-hhv071017.php
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4758194/
https://medicalxpress.com/news/2017-08-virus-mono-ms-multiple.html
Regards,
Joachim
Agreed, any form of toxic stress can trigger mutated mast cells (mMC) into an inflammatory cascade. Mast cells are on all cutaneous tissue. In MS, the mMC find molecular mimicry on the optic nerve, two areas of the brain and the cervical spine. PGD2 increases histemic inflammation up to 1000 times, allowing for violation of both the BBB and lymphatic vasculature in the CNS.
It does not work that way! Firstly, it does not explain the PPMS, where there is no inflammation. Secondly, it does not explain the conversion of RRMS into SPMS. Thirdly, the Oligoclonal (IgG) Bands found in the CSF are not directed towards any particular virus or even any particular myelin protein. It is true that one can induce EAE in mice using MBP and MOG, but the IgG found in the CSF do not seem to be antibodies against either of these proteins. Molecular mimicry is a hypothesis used for inducing EAE in mice, but we still do not know for sure against which protein these IgG antibodies are being produced in RRMS. Lastly, it has been shown in many studies that "stress" does not cause any type of MS. We actually give massive doses of steroids (the stress hormone) to treat MS relapse. MS in general and RRMS in particular is not entirely an autoimmune disease as the treatments are at most 50% effective only, except Tysabri which is about 70%. thanks, Mustafa.
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