Figure 1.

Inhibition of virus infectivity by APO3G. Cells restrictive for the replication of Vif-defective HIV express the cytidine deaminase APOBEC3G (APO3G). In the absence of Vif, APO3G is packaged into virus particles (1). Such virions are capable of penetrating a target cell and initiate minus-strand cDNA synthesis ((-)-cDNA). However, APO3G causes hypermutation of the viral (-)-cDNA resulting in the conversion of deoxycytidine to deoxyuridine (2). Deoxyuridine residues in the viral cDNA can be targeted by uracil-DNA glycosylase, which could lead to endonucleolytic cleavage by endonucleases present in the target cell (3). Alternatively, hypermutated cDNA enters the nucleus (4) and integrates into the host genome but results in the production of defective or aberrant viral proteins (5). This can lead to an impairment of virus assembly or result in the assembly of non-infectious viruses (6).