RIPK1 and infection: In all three cases, treatment with a PR inhibitor prevented cleavage of the cellular protein; moreover, inhibition of either reverse transcription or integration completely abrogated RIPK1 cleavage after infection of Sup-T1 cells with HIV-1 NL4.3, proving that RIPK1 was mainly cleaved by post-integration expressed PR rather than by PR present in incoming virions.