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