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. Author manuscript; available in PMC: 2020 Jul 15.
Published in final edited form as: Trends Mol Med. 2018 Mar 30;24(5):507–520. doi: 10.1016/j.molmed.2018.03.004

Figure 1. A schematic depiction of the potential interactions between Vif, A3G and E3 ubiquitin ligase complex in the pathway by which Vif shuttles A3G to the proteasome for degradation.

Figure 1

‘Block Vif/Vif’, ‘Block A3G/Vif’ and ‘Block Vif/EloC’ call out where small molecule inhibitors have been proposed to effect in the Vif-dependent A3G degradation pathway, whereas ‘Block/CBFβ’ is another possible target with no inhibitors discovered to date. If Vif is not blocked from functioning HIV particles are released from cells leading to ‘active infection’ and propagation of the virus to more cells (left, white and blue arrows). When Vif is blocked, A3G abundance is maintained and it is packaged into virions leading to ‘inhibited infection’ via A3G’s ability to hypermutate HIV DNA during reverse transcription leading to unintegrated and non-functional HIV DNA with dG to dA hypermutations (right, black and yellow arrows).