ikulo wrote:I'm not sure if this was discussed somewhere else at some point. But, I'm wondering how the virus theory fits in with the immune suppressant medications MSers take. What I mean is -- if MS were caused by a virus, would taking DMDs (or even chemo-type drugs that kill the immune system) allow this virus to run rampant in our bodies thereby making us even worse? Or do retroviruses work differently? Any ideas?
ikulo wrote:But my question is this... the body's immune system is designed to protect the body from viruses. But if the immune system has been shut down with chemo, wouldn't this allow the hypothetical "MS Virus" to replicate and do further damage? maybe viruses are killed by different immune cells? hm.
AVONEX@ has a specific activity of approximately 200 million international units of antiviral activity per mg; 30 mcg of AVONEX@ contains 6 million IU of antiviral activity.
Interferons are a family of naturally occurring proteins and glycoproteins that are produced by eukaryotic cells in response to viral infection and other biological inducers. Interferon beta, one member of this family, is produced by various cell types including fibroblasts and macrophages.
Interferons are cytokines that mediate antiviral, antiproliferative and immunomodulatory activities in response to viral infection and other biological inducers.
Interferon Beta is a cytokine produced by a wide variety of cells; a host cell encountering Interferon Beta becomes much less likely to be infected by a virus.
Bryan Grenfell and collaborators have now investigated how Interferon Beta can affect the spatial spread of viral infections within a host.
Using an in vitro experimental system, the researchers inoculated monolayers of host cells with Herpes simplex virus 1 (pictured).
The researchers produced a simple mathematical model that described the observed experimental data. This is one of the first models of within-host spatial interactions between viruses and cytokines.
- The virus killed some cells; daughter virions then moved to infect nearby cells. Thus, plaques of dead host cells formed.
- The growth of the plaques was eventually halted and reversed as the host cells began to produce Interferon Beta.
- The maximal area of the plaque and the time to recover depended on the quantity of virus in the inoculum and on the amount of Interferon Beta in the system.
CLINICAL USE AND SIGNIFICANCE
Vitamin D3 and some metabolically active precursors are potent inducers of the synthesis of NGF at concentrations of 100 picoM. This may have implications for the treatment of neurodegenerative diseases with NGF.
The infusion of human NGF into brains of primates has been shown to prevent the degeneration of cholinergic neurons. It may be possible, therefore, to use NGF to protect cholinergic neurons in Alzheimer's disease which is characterized by a selective degeneration of these cells. Another possible application might be the treatment of diabetes-associated polyneuropathies. In experimental animals NGF prevents chemotherapy induced neuropathies.
ikulo wrote:Thanks for the info JackD. I will definitely put on my research hat and read up on all this.
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