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Although the mechanisms by which TRIM5α can induce the abortive disassembly of retroviral capsids have remained obscure, numerous studies have suggested a role for ubiquitination and cellular degradative pathways. These studies have typically relied on global perturbation of cellular degradative pathways. Here, through the use of linkage-specific deubiquitinating enzymes tethered to TRIM5α, we delineate the ubiquitin linkages which drive specific steps in restriction and degradation by TRIM5α, providing evidence for a noncanonical role for K63-linked ubiquitin in the process of retroviral restriction by TRIM5α and potentially providing insight into the mechanism of action of other TRIM family proteins.

K63-Linked Ubiquitin Is Required for Restriction of HIV-1 Reverse Transcription and Capsid Destabilization by Rhesus TRIM5α