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Prof Pender has come up with a theory linking EBV and Vit D with MS.

Full article below:

http://nro.sagepub.com/content/early/20 ... l.pdf+html

Ian

Great paper, Ian--thanks for posting. EBV is most certainly a part of the puzzle and this is a well-reasoned hypothesis.

I have my own hypothesis as to how latent EBV (present in 95% of the adult population) becomes reactivated in the MS brain, and why it is present in the MS brain but not in other neurodegenerative diseases--maybe diffuse cerebral hypoxia due to venous insufficiency.
http://www.ncbi.nlm.nih.gov/pubmed/16931136

Hypoxia treatment not only increased the expression of the EBV immediate-early protein Zta (which mediates the switch between the latent and lytic form of infection), but also increased the number of EBV DNA copies in B95-8 cells.
Conclusions
EBV in latent infection can be activated to lytic infection by hypoxia treatment.

One such virus that displays this characteristic is the lymphotropic human herpesvirus, Epstein-Barr virus (EBV). EBV is latent in B-cells that exist in the peripheral circulation as non-dividing memory B-cells; within lymph nodes EBV-infected cells become proliferating blasts that secrete antibody [19,20] . These two dramatically distinct cellular phenotypes result from two different viral gene expression patterns during latency [ibid]. Recent results indicate that the EBV transactivator, Epstein-Barr nuclear antigen 1 (EBNA1), is regulated by oxygen tension [18] . Under hypoxic or reducing conditions, EBNA1 is active as a transactivator and drives viral gene expression required for cell proliferation. For EBNA1, the redox state of a pair of cysteines in a conserved cys-x-x-cys motif governs its ability to transactivate

http://www.virologyj.com/content/7/1/93
Who knows? Maybe more studies someday--
cheer

Cheer - Nice theory but I'd be more convinced if either of those articles mentioned MS or CCSVI. As is I see some huge leaps of faith being made to fill in the blanks.

I prefer my more drastic, even less proven approach of bone marrow transplants from EBV free matching donors.

Pender is on the right track but barking up the wrong tree. I've long been a believer that herpes is a big factor in MS. Several members of the herpes family have strong associations with MS - not just EBV. I find Pender's slant on EBV unbelievably complex, and complexity in research is often used to cover up weaknesses in theories, or lack of real evidence.

How does he account for places like Sicily which is one of the world's MS (and herpes) hotspots, despite the massive dose of vitamin D from sunshine? (Malta, almost next door, has dramatically less MS incidence).

Researchers often attempt to find evidence of EBV, or other herpes virus attack on nerve tissue during an MS attack, but this has never, repeat never been found. My theory is that the mere presence of the inactive herpes virus "scares" or stimulates the immune system into launching an attack on healthy tissue in the locality of the virus. For me, this explains why a Mexican study (2008) found that herpes (varicella-zoster) DNA increased in the spinal fluid by over 500 times during MS attacks. VZV DNA was not found in the spinal fluid of any of those who did not have MS.

http://www.ncbi.nlm.nih.gov/pubmed/18306233


Stress often triggers herpes (which lives dormant in the nerve ganglia). Stress often triggers MS.

In both cases we dont know why......maybe its something to do with what stress does to herpes in the actual nerves.



gainsbourg