HIV-related mortality has fallen due to scale-up of antiretroviral therapy (ART), so more women living with HIV (WLH) now live to reach menopause. Menopausal estrogen loss causes bone loss, as do HIV and certain ART regimens. However, quantitative bone data from WLH are few in Africa. A cross-sectional study of women aged 40-60 years (49% WLH) was conducted in Harare, Zimbabwe. Menopause status, fracture history, HIV status and treatment, and anthropometry were collected, and radial/tibial peripheral Quantitative Computed Tomography (pQCT) scans performed. pQCT outcomes were: distal radius and tibia trabecular volumetric bone mineral density (vBMD), total area, and compressive bone strength (BSIc); proximal radius and tibia cortical vBMD, bone mineral content (BMC), cortical thickness, bone area, and stress-strain index (SSI). Linear regression determined differences by HIV status, minimally adjusted for age and menopause status, and further adjusted for height and fat mass. Relationships between pQCT parameters and major osteoporotic fracture history were explored using univariate logistic regression. In WLH, linear regression assessed associations between HIV and ART durations on pQCT measures. 384 women mean(SD) age 49.7(5.8) years had pQCT data. WLH had lower absolute pQCT measures at all sites. Overall, HIV-related deficits were robust to adjustment for age, menopause status, height, and fat mass: WLH had lower trabecular vBMD (radius -7.3 [-12.5; -2.0]%, tibia -5.4 [-9.1; -1.7]%), and cortical vBMD (radius -3.5 [-5.9; -1.1]%, tibia -1.1[-1.6; -0.5]%). Strength estimates were lower in WLH and of similar magnitude at the radius and tibia. Longer HIV duration was associated with lower radius bone area, BMC, estimates of bone strength, independent of ART duration. Trabecular deficits predominate in WLH, though with age cortical compartment bone loss may increase in importance. This is particularly concerning as these differences were observed at the radius, a common site of postmenopausal osteoporotic fracture.