squiffy2 wrote:Absence of Epstein-Barr virus in the brain and CSF of patients with multiple sclerosis - http://www.msrc.co.uk/index.cfm/fuseact ... pageid/707
Actually, those findings don't surprise me because I believe the researchers are looking up the wrong tree. They are making the assumption that they need to find evidence of herpes attack .... but maybe there isn't any attack even though we know that herpes antibodies are produced in MS.
In war, an invading army doesn't necessarily need to fire a single shot in order to provoke a massive defensive bombardment - purely because it is considered to be a threat. That's what is maybe happening in MS, the presence of herpes hiding and cloaking itself deep in nerve tissue (in one shape or another) is enough to trigger a defensive response. This is mistaken as being the body attacking itself, in other words what seems to be an autoimmune response.
The Sargsyan study confirmed previous findings that herpes antibodies are there:
"Anti-EBV antibodies were detected in the CSF of patients with MS"
This latest research ignores the fact that herpes antibodies are not found in the CSF of those without MS, or the fact that herpes antibodies (VZV at least) are known to increase in the CSF during MS attacks. Discoveries about herpes have been coming in thick and fast in the last few years. Locating it and understanding it seems to be as complicated as HIV. New discoveries are being made all the time - so don't rule it out just yet!
BioDocFL wrote:I think what we will find is that many different pathogens can trigger an autoimmune reaction by affecting cells in a local environment, so we are not going to find one culprit virus that we can blame everything on. I believe that EBV just happens to be the most effective at it because it gets into B cells (and other cell types) easily and affects that host cell.
The frequency of detected intrathecal anti-EBV antibody synthesis in patients with MS did not differ from that in non-MS inflammatory CNS disease control patients.
Stress-related immune suppression: health implications (Glaser 1987)
This study used a year-long prospective design to assess linkages among distress, immunity, and illness. Serial blood samples were collected from 40 first-year medical students at the first, third, and fifth examination periods, as well as 1 month before each. There were significant decrements in the production of gamma-interferon by concanavalin A-stimulated lymphocytes obtained at the time of examinations. Antibody titers to Epstein-Barr virus (EBV) increased during examination periods, suggesting reactivation of latent EBV and therefore poorer cellular immune control of latent virus. We obtained data that suggest that T-cell killing by memory T lymphocytes of EBV transformed autologous B lymphocytes also declined during examination periods. The activity of a lymphokine, leukocyte migration inhibition factor, normally suppressed during recrudescence of herpes simplex virus type 2 infections, was altered during examination periods and an increase in both plasma and intracellular levels of cyclic AMP associated with examination stress was observed. An increase in the incidence of self-reported symptoms of infectious illness was also associated with examination periods. The data support the linkage between stress-related immunosuppression and health.
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