Introduction: Atazanavir inhibits UDP-glucuronyl-transferase-1A1 (UGT1A1), which metabolizes raltegravir, but the magnitude of steady-state inhibition and role of UGT1A1 genotype is unknown. Sufficient inhibition could lead to reduced-dose and -cost raltegravir regimens. Methods: Nineteen healthy volunteers, age 24 - 51 years, took raltegravir 400 mg twice daily (treatment Arm A) and raltegravir 400 mg plus atazanavir 400 mg once daily (treatment Arm B). Each treatment arm was separated by ≥3 days. After one week on each regimen, raltegravir and raltegravir-glucuronide plasma and urine concentrations were measured by liquid chromatography-tandem mass spectrometry in multiple samples obtained over 12 hours (Arm A) or 24 hours (Arm B) and analyzed by non-compartmental methods. UGT1A1 promoter variants were detected with a commercially available kit and published primers. The primary outcome was the ratio of plasma raltegravir Ctau, or concentration at the end of the dosing interval for Arm B (24 hours) vs. Arm A (12 hours). Frequentist and Bayesian distributions of this ratio were compared. Results: The Arm B to Arm A geometric mean ratios (GMR) and 95% confidence intervals for plasma raltegravir Ctau, AUC0-12, and raltegravir-glucuronide:raltegravir AUC0-12 were 0.38 (0.22 - 0.65), 1.32 (0.62 - 2.81), and 0.47 (0.38 - 0.59), respectively. Using results from a previously published study of single-dose raltegravir added to atazanavir as a prior distribution, the Bayesian posterior GMR and 95% credibility interval for the Arm B to Arm A Ctau ratio was 0.28 (0.19 - 0.41). Nine volunteers were heterozygous and one was homozygous for a UGT1A1 reduction-of-function allele, but these were not associated with metabolite formation. Conclusions: Although atazanavir significantly reduced formation of the glucuronide metabolite, its steady-state boosting of plasma raltegravir did not render Ctau with a once-daily raltegravir dose of 400 mg similar to Ctau with the standard twice-daily dose, regardless of frequentist or Bayesian analytic methods. UGT1A1 promoter variants did not significantly influence this interaction.