HIV-1 Evolution Following Transmission to an HLA-B*5801- Positive Patient

The human immunodeficiency virus type 1 (HIV-1)–specific immune responses of patients with the HLA-B*57/5801 al-leles who spontaneously control viral replication serve as an important model for T cell–based HIV-1 vaccines. Deter-mining the breadth of this response and the extent of vi-rologic escape in primary infection in these patients is there-fore critical. Here we document the development of mutations in 3 HLA-B*5801-restricted epitopes in gag, nef, and pol in an HLA-B*5801-positive patient who had a viral load of only 1159 copies/mL at day 167 after infection. A full genome sequence analysis was performed to determine the extent of mutations in HLA-B*5801-restricted epitopes, and longitudinal sequence data of specific genes were combined with enzyme-linked im-munospot assay analysis of critical epitopes to determine the importance of escape mutations. Thus, relative control of viral