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Re: cjgaddy post# 47048

Friday, 01/15/2010 12:47:55 PM

Friday, January 15, 2010 12:47:55 PM

Post# of 346050
cj, thanks. Tony Moody, at Duke, used anti-PS MABs taken from auto-immune disease patients, and confirmed that [in a test tube] the Anti-PS MABs “neutralized” virus, or decreased viral cell entry, and the mechanism was via release of cell-synthesized chemical attractant compounds called “chemokines.” The specific chemokines, called MIP1a and MIP1b, are chemicals secreted by monocytes, the white blood cell scavengers. The chemokines (MIPs)dock on, or attach to, cell membrane receptors (docking sites), plugging the porthole in the cell membrane [receptor site] through which HIV enters a cell, That docking site is called the CCRF receptor. Evidence in favor of the conclusion: Moody found that “neutralization” of virus infection could be reversed by antibodies directed against the MIP1a and MIP1b, concluding that the mechanism of action of anti-lipid antibodies is that they stick to the host target cell and not the virus to prevent infection, and that a vaccine that induces such antibodies may not be able to directly neutralize HIV but may reduce virus spreading.


Tony Moody of Duke Univ. School of Medicine used anti-lipid monoclonal antibodies taken from patients with auto-immune disease, and confirmed that [in a test tube] the Anti-PS MABs “neutralized” virus, or decreased viral cell entry, and found that the probable mechanism was via release of cell-synthesized chemical attractant compounds called “chemokines.” Chemokines use chemical signals as attractants to other immune cells. The specific chemokines released by the antiPS MABs are called MIP1a and MIP1b, and are secreted by monocytes, the white blood cell scavengers. These chemoattractants dock on, or attach to, cell membrane receptors (docking sites), plugging the port-hole in the cell membrane [receptor site] through which HIV enters a cell, That docking site is called the CCRF5 receptor. Moody found that “neutralization” of virus infection could be reversed by antibodies directed against the MIP1a and MIP1b, concluding that the MOA of anti-lipid antibodies is that they stick to the host target cell and not the virus to prevent infection. A vaccine that induces such antibodies may not be able to directly neutralize HIV but it may reduce virus spreading
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