Additional concerns regarding continuous ART are the induction of drug resistance, high costs, and treatment fatigue in patients. Structured treatment interruption (STI) strategies have therefore been explored in patients with viral replication suppressed under ART [3-6]. Overall, results were disappointing, with a significant

AZD1152-HQPA cell line proportion of patients showing rapid increases in viral load, declining CD4 T-cell counts, and an increased risk for disease progression [4, 7]. However, a subgroup of patients are able to suppress HIV replication for prolonged periods of time after STI [8]. A marker identifying such patients would be of great practical value and might renew interest in STI. Several studies have identified genetic factors influencing the pretreatment set-point viral load and time to progression to AIDS in untreated patients: the first locus identified was human leucocyte antigen (HLA)-B [9]. The natural killer (NK) cell receptor pair killer cell immunoglobulin-like receptor 3DL1 (KIR3DL1)/KIR3DS1 followed [10]. More recently, whole-genome association studies provided the information that two single nucleotide polymorphisms, found in or close to the HLA complex, both correlate with HIV viral load in untreated individuals [11]. The

first (rs9264942) is located 35 kbp upstream of HLA-C (HLA-C −35 C/T) and governs the level of surface expression of HLA-C [12]. The second (rs2395029) buy Y-27632 lies in the HLA complex P5 (HCP5) and is in strong linkage disequilibrium with HLA B*5701, the HLA-B allele associated with the strongest protection from disease progression. Interestingly, all of

these polymorphisms are potentially associated with the function of NK cells, a subgroup of lymphocytes important in defence against viral infection: KIR3DL1 is an inhibitory receptor binding HLA-B antigens that carry the Bw4 epitope [13]. HLA-C is the ligand for the NK cell receptors KIR2DL1, KIR2DL2, KIR2DL3 and KIR2DS1 [14]. KIR–HLA interactions are important during NK cell development, as only NK cells carrying inhibitory KIR and their HLA ligands acquire full functional competence [15]. As antiviral effects of NK cells have been shown to operate most effectively in states of low viral load [16], we hypothesized that these polymorphisms may have a role in predicting Urease which patients are able to maintain suppressed viral load after STI. We therefore studied the association of these polymorphisms with the evolution of viral load after STI in 130 Swiss HIV Cohort Study patients. Patients were recruited from Swiss HIV Cohort Study participants of the Strategies for Management of Anti-Retroviral Therapy (SMART), Swiss Spanish Treatment Interruption Trial (SSITT)/2nd SSITT, and STACCATO (A Trial of CD4 Guided Treatment Interruption, Compared to Continuous Treatment, for HIV Infection) trials [3-6].