DEATH ASSOCIATED WITH GP120 BINDING FOR CCR5

Not only does gp120 cause cell death in uninfected host immune cells through Fas-dependent mechanisms as a result of binding CD4’ but it also does this through binding and signaling through chemokine co-receptors alone.

The gp120 can bind to CCR5 or CXCR4 without first binding the CD4 receptor’ and such binding ultimately signals cell death. In the case of CCR5 binding and signaling, gp120 makes the CD4⁺ T cell susceptible to Fas-mediated killing. The resulting apoptosis can be abrogated by preventing gp120 from binding to CCR5 with antibodies, β-chemokines that are natural ligands for the CCR5 receptor, or nonactivating small molecule inhibitors that bind CCR5 and block gp120 binding.^9,58 Because cell death is Fas mediated and signals through the caspase cascade, the death caused by HIV signaling through CCR5 can also be blocked by inhibiting the caspase cascade. It is unclear whether the CCR5 chemokine receptor signals these messages alone or whether it acts in concert with CD4. When CCR5 is engaged by a ligand, it rafts with the CD4 receptor.⁵⁹ Therefore, it is possible that gp120 activation of CCR5 is actually signaling a caspase-dependent death to the cell via CD4 signaling.

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