FIGURE 2.

Potential effects of A3-mediated mutagenesis on CTL responses. A3F- and A3G-mediated mutagenesis alters CTL responses through the accumulation of G-to-A mutations on the viral genome, which leads to the modification of epitope sequences and their flanking regions involved in antigen processing/presentation, HLA binding, and TCR recognition. The two examples show that A3-mediated hypermutation on epitope sequences potentially alters HLA binding of the epitopes and TCR recognition. Sublethal A3-mediated mutagenesis is involved in the emergence of CTL escape variants (top), whereas lethal A3-mediated hypermutation likely increases the number of HIV-derived epitopes and consequently enhances HIV-1-specific CTL responses (bottom). A3, APOBEC3; CTL, cytotoxic T lymphocyte; HLA, human leukocyte antigen; TCR, T cell receptor.