FIG 6.

Schematic model of the effects of proteasome inhibitors of HIV-infected cells. Proteasome inhibitors directly induce viral replication, which generates Casp8p41, which is bound and inhibited by Bcl2 and then targeted to the proteasome for degradation. Proteasome inhibitor-mediated blockade of Casp8p41 degradation favors accumulation of Casp8p41, which overcomes Bcl2 restriction, causing death of the reactivated, infected cell. Because Casp8p41 is not present in uninfected cells, this pathway does not operate in uninfected bystander cells.