HLA‐Bw4 identifies a population of HIV‐infected patients with an increased capacity to control viral replication after structured treatment interruption

Objectives After structured treatment interruption (STI) of treatment for HIV‐1, a fraction of patients maintain suppressed viral loads. Prospective identification of such patients might improve HIV‐1 treatment, if selected patients are offered STI. Methods We analysed the effect of previously identified genetic modulators of HIV‐1 disease progression on patients’ ability to suppress viral replication after STI. Polymorphisms in the genes killer cell immunoglobulin‐like receptor 3DLI (KIR3DL1)/KIR3DS1, human leucocyte antigen B (HLA‐B) and HLA Complex P5 (HCP5), and a polymorphism affecting HLA‐C surface expression were analysed in 130 Swiss HIV Cohort Study patients undergoing STI. Genotypes were correlated with viral load levels after STI. Results We observed a statistically significant reduction in viral load after STI in carriers of HLA‐B alleles containing either the Bw480Thr or the Bw480Ile epitope (mean adjusted effect on post‐STI viral load: −0.82 log HIV‐1 RNA copies/ml, P