Thus, V3-CCR5 signaling acts as a double-edged sword; V3 renders cells hyper-responsive to stimulation favoring HIV infection and vigorous T cell proliferation, but in the case of an abortive entry of HIV into a T cell, the cell undergoes sustained proliferation but is condemned to AICD due to the absence of Nef to balance the homeostatic mechanisms of apoptosis. This evidence concerns the gene S100B and HIV infectious disease.