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Different signal transduction events induced in normal lymphocytes versus transformed T-cells by HIV.




 

Int Conf AIDS. 1993 Jun 6-11;9(1):186 (abstract no. PO-A14-0312). Unique

The T lymphocyte surface protein, CD4, is the primary receptor for HIV, and it binds the viral surface glycoprotein, gp120. As a receptor for class II MHC molecules, CD4 functions as a signal transducer via tyrosine phosphorylation. Previous studies have shown discrepant results concerning the effect of HIV infection on cellular signal transduction, with some indicating that HIV activates certain signal transduction cascades while other studies indicate that it inhibits such events. We examined whether HIV infection could induce phosphatidylinositol (PI) signal transduction in both transformed T cells and normal peripheral blood lymphocytes (PBLs). We found that HIV infection of, or binding of HIV, per se, to transformed T cells did not induce a typical PI signal transduction. Rather it appeared to specifically inhibit PIP kinase. In contrast, HIV infection of resting PBLs induced normal PI signal transduction, resulting in activation of phospholipase C. These results show that one should be careful in extrapolating results from transformed cells to that of normal cells, and that there is a difference in these pathways in the two cell types.

*Antigens, CD4/PHYSIOLOGY *Cell Transformation, Neoplastic *HIV/PHYSIOLOGY *Phosphatidylinositols/PHYSIOLOGY *Signal Transduction *T-Lymphocytes/PHYSIOLOGY



 




Information in this article was accurate in November 30, 1993. The state of the art may have changed since the publication date. This material is designed to support, not replace, the relationship that exists between you and your doctor. Always discuss treatment options with a doctor who specializes in treating HIV.