The Stat1/Vitamin A Theory of AIDS
In a previous Blog, I discussed the importance of the STAT1 signaling pathway in the development of AIDS.
http://grouppekurosawa.com/blog/2006/01/egcg-and-treatment-of-hiv.htm
This essay quickly reviewed the role of STAT1 in the immune dysfunction and organ failure associated with AIDS.
In the last few weeks, the information pipeline on this topic has "runneth over".
It is now clear that low vitamin D3 status, both availability from the skin and conversation to active 1,25 Vit D3, AND enhanced STAT1 activation due to viral NEF and gp120 proteins, AND vitamin A or retinoic acid can account for the immune dysfunction that prevents the clearance of the HIV virus from the body.
A few points.
1. STAT1 binds directly to the vitamin D3 receptor, VDR, and prevents its interaction with the vitamin A receptor RXR, as discussed in the previous Blog. This means that STAT1 activation blocks vitamin D3 activity.
2. Both STAT1 and retinoic acid are necessary to induce the death pathway TRAIL. TRAIL, and only TRAIL, is responsible for the activation induced cell death and apoptosis of non-infected CD4 T cells.
3. Retinoic acid activates macrophages and dendritic cells along certain pathways. Naive T cells that bind retinoic acid stimulated accessary cells produce ONLY Th2 CD4 T cells. These T cells cannot kill virally infected cells.
4. HIV can only replicate in Th2 T cells.
5. Retinoic acid causes TNF alpha mRNA to become unstable. TNF is absolutely necessary for the clearance of virus and other pathogens.
6. Retinoic acid induces a state of latency in HIV infected macrophages. Cells that have latent viral infections cannot be killed, thereby perpetuating the infection over a long period of time.
It is becoming clear that STAT1 activation by NEF and gp120 inhibit vitamin D3 responsiveness. Since vitamin D3 antagonizes many of the biological effects of vitamin A, this promotes vitamin A responsiveness by default. This shift the immune response toward Th2, a response that promotes allergy but cannot kill virally infected cells. This accounts for the failure of delayed hypersensitivity responses so quickly after infection, and the eventual problems associated with reduced bone density.
EGCG is the only known natural medicine that can inhibit STAT1. Therefore a treatment protocol for the earlier phases of HIV infections should include EGCG, melatonin (to block viral VPR activity and promote cell mediated immunity), and vitamin D3 plus calcium.
Vitamin A supplements should not be used, nor should people consume high vitamin A containing foods such as liver.
More to come.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
(http://www.grouppekurosawa.com)
http://grouppekurosawa.com/blog/2006/01/egcg-and-treatment-of-hiv.htm
This essay quickly reviewed the role of STAT1 in the immune dysfunction and organ failure associated with AIDS.
In the last few weeks, the information pipeline on this topic has "runneth over".
It is now clear that low vitamin D3 status, both availability from the skin and conversation to active 1,25 Vit D3, AND enhanced STAT1 activation due to viral NEF and gp120 proteins, AND vitamin A or retinoic acid can account for the immune dysfunction that prevents the clearance of the HIV virus from the body.
A few points.
1. STAT1 binds directly to the vitamin D3 receptor, VDR, and prevents its interaction with the vitamin A receptor RXR, as discussed in the previous Blog. This means that STAT1 activation blocks vitamin D3 activity.
2. Both STAT1 and retinoic acid are necessary to induce the death pathway TRAIL. TRAIL, and only TRAIL, is responsible for the activation induced cell death and apoptosis of non-infected CD4 T cells.
3. Retinoic acid activates macrophages and dendritic cells along certain pathways. Naive T cells that bind retinoic acid stimulated accessary cells produce ONLY Th2 CD4 T cells. These T cells cannot kill virally infected cells.
4. HIV can only replicate in Th2 T cells.
5. Retinoic acid causes TNF alpha mRNA to become unstable. TNF is absolutely necessary for the clearance of virus and other pathogens.
6. Retinoic acid induces a state of latency in HIV infected macrophages. Cells that have latent viral infections cannot be killed, thereby perpetuating the infection over a long period of time.
It is becoming clear that STAT1 activation by NEF and gp120 inhibit vitamin D3 responsiveness. Since vitamin D3 antagonizes many of the biological effects of vitamin A, this promotes vitamin A responsiveness by default. This shift the immune response toward Th2, a response that promotes allergy but cannot kill virally infected cells. This accounts for the failure of delayed hypersensitivity responses so quickly after infection, and the eventual problems associated with reduced bone density.
EGCG is the only known natural medicine that can inhibit STAT1. Therefore a treatment protocol for the earlier phases of HIV infections should include EGCG, melatonin (to block viral VPR activity and promote cell mediated immunity), and vitamin D3 plus calcium.
Vitamin A supplements should not be used, nor should people consume high vitamin A containing foods such as liver.
More to come.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
(http://www.grouppekurosawa.com)
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