January 22, 2012 at 10:06am
Perhaps researchers need to look more closely at hypoperfusion, or slowed cerebral blood flow, in MS. Lower levels of oxygen can affect the brain in many ways.
There has been much made about the connection of the Epstein Barr virus (EBV) and MS. Most people carry the latent, or dormant version of this virus. Nearly 95% of all adults carry the EBV virus.
A recent post mortem study showed reactivated EBV cells in active MS lesions.
In the seven MS patients' postmortem brain tissue studied, active MS lesions all contained Epstein-Barr virus infected cells.
Such cells weren't unique to MS, but were also detected in CNS tissue from two control patients with stroke, which the researchers pointed out is also a disease in which inflammation plays an important role.
Notably, Epstein-Barr virus-positive cells were present in much higher numbers in active MS lesions than expected in peripheral blood B cells, "which suggests that these cells are recruited to or accumulate in CNS infiltrates," Lünemann noted.
What might reactivate this virus and cause it to replicate in the B cells?
Why were these cells also in the brains of stroke patients? It's not just about inflammation or the immune system.
Hypoxia. Lack of oxygen reactivates EBV infection. The ischemic injury of slowed blood flow, caused be stroke or CCSVI, could reactivate EBV cells.
EBV in latent infection can be activated to lytic infection by hypoxia treatment.
In fact, researchers have found a link between pwMS who smoke, and the levels of EBV antigens, or ENBA titers.
The investigators found that among patients with MS, anti-EBNA titers were much higher among smokers than among nonsmokers. In addition, the increased risk of MS associated with anti-EBNA was stronger among those who had ever smoked (odds ratio [OR], 3.9; 95% confidence interval [CI], 2.7 – 5.7) compared with never smokers (OR, 1.8; 95% CI, 1.4 – 2.3; P value for interaction = .001).
By contrast, the association between smoking and MS was not present in individuals with low anti-EBNA titer levels. In addition, the risk of MS associated with smoking did not appear to be modified by HLA-DR15 gene status.
To my knowledge, there is not a well-described causative mechanism linking smoking and MS,” she said. “Possible mechanisms, such as neurotoxicity and immunomodulatory effects, have been suggested, but there is limited data on this topic.”
Asked for comment on these findings, Lily Jung, MD, with the Swedish Neuroscience Institute, in Seattle, Washington, added that recent studies show that not only does smoking increase risk of developing MS, it also increases magnetic resonance imaging lesion volume and brain atrophy and leads to faster progression of the disease.
But the researchers cannot comment on how cigarette smoking would increase EBV, increase brain atrophy and worsen MS?
Smoking decreases oxygen and increases hypoxia. Hypoxia activates EBV.
Please put the pieces together, MS researchers.
Look at O2 levels in MS brains. Study hypoperfusion.
Look at blood flow.
THANK YOU always for your posts.ReplyDelete
Lynnie in the UK