CCR5 and HIV infectious disease: 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.