AID Hotspot Mutagenesis: Somatic Hypermutation

This simulation renders a real 3D double helix standing in for an antibody V-region gene and drives it with the actual molecular logic of somatic hypermutation: AID scans the exposed strand and deaminates cytosine to uracil far more often inside WRC/RGYW hotspot motifs than elsewhere, matching the sequence bias measured in real B cells. Each uracil then resolves through one of two competing repair outcomes you control the balance of — faithful replication over the lesion, which fixes a clean C:G → T:A transition, or error-prone base-excision/mismatch repair, which tends to produce transversions and spreads mutations onto neighbouring A:T bases. Live readouts track total mutations, the fraction landing on true hotspot motifs, and the transition:transversion ratio, so you can watch the characteristic SHM mutation spectrum emerge from the underlying biochemistry before any affinity-based selection is applied.