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We evaluated treatment duration and viral suppression (VS) outcomes with integrase strand transfer inhibitor (INSTI)-based regimens versus other contemporary regimens among adults in routine HIV care. Eligible participants were seen during January 1, 2007 to June 30, 2018 at nine U.S. HIV clinics, initiated antiretroviral therapy (ART) (baseline date), and had ≥2 clinic visits thereafter. We assessed the probability of remaining on a regimen and achieving HIV RNA <200 copies/mL on initial INSTI versus non-INSTI ART by Kaplan–Meier analyses and their correlates by Cox regression. Among 1,005 patients, 335 (33.3%) were prescribed an INSTI-containing regimen and 670 (66.7%) a non-INSTI regimen, which may have included non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and other agents. In both groups, most patients were male, nonwhite, and aged <50 years. Comparing the INSTI with non-INSTI group, the median baseline log10 HIV viral load (VL; copies/mL) was 4.6 versus 4.5, and the median CD4+ cell count (cells/mm3) was 352 versus 314. In Kaplan–Meier analysis, the estimated probabilities of remaining on initial regimens at 2 and 4 years were 58% and 40% for INSTI and 51% and 33% for non-INSTI group, respectively (log-rank test p = .003). In multivariable models, treatment with an INSTI (vs. non-INSTI) ART was negatively associated with a regimen switch [hazard ratio (HR) 0.67, 95% confidence interval (CI) 0.56–0.81, p < .001] and was positively associated with achieving VS (HR 1.52; CI 1.29–1.79, p < .001), both irrespective of baseline VL levels. Initial INSTI-based regimens were associated with longer treatment durations and better VS than non-INSTI regimens. Results support INSTI regimens as the initial therapy in U.S. treatment guidelines. [ABSTRACT FROM AUTHOR]

To explore reasons for the disproportionate metabolic and cardiovascular disease burdens among older HIV-infected persons, we investigated whether associations of CD4 count and HIV viral load (VL) with non-high-density lipoprotein cholesterol (non-HDL-C) and high-density lipoprotein cholesterol [HDL-C] differed by age. Longitudinal clinical and laboratory data were collected between 2011 and 2016 for HIV-infected outpatients in the DC Cohort study. Using data for patients aged ≥21 years with ≥1 cholesterol result and contemporaneous CD4/VL results, we created multivariable linear regression models with generalized estimating equations. Among 3,912 patients, the median age was 50 years, 78% were male, 76% were non-Hispanic black, 93% were using antiretroviral therapy, 8% had a CD4 count <200 cells/μL, and 18% had an HIV VL ≥200 copies/mL. Overall, CD4 count <200 (vs. >500) cells/μL and VL ≥200 copies/mL were associated with lower non-HDL-C concentrations (p < .01), but associations were more positive with increasing age (CD4–age/VL–age interactions, p < .01). CD4 count <200 cells/μL was associated with lower non-HDL-C among patients aged <50 years [β = −7.8 mg/dL (95% confidence interval, CI: −13.2 to −2.4)] but higher non-HDL-C among patients aged 60–69 years [β = +8.1 mg/dL (95% CI: 0.02–16.2)]. VL ≥200 copies/mL was associated with lower non-HDL-C among patients aged <50 years [β = −3.3 mg/dL (95% CI: −6.7 to 0.1)] but higher non-HDL-C among patients aged ≥70 years [β = +16.0 mg/dL (95% CI: −1.4 to 33.3)], although precision was reduced in age-stratified analyses. Although no age differences were detected for HDL-C, VL ≥200 copies/mL was more strongly associated with lower HDL-C concentrations when CD4 count was <200 cells/μL [β = −7.0 mg/dL (95% CI: −9.7 to −4.3)] versus 200–500 cells/μL [β = −4.2 (95% CI: −5.9 to −2.6)] or >500 cells/μL [β = −2.2 (95% CI: −3.7 to −0.8)] (CD4–VL interaction, p < .01). We detected a novel age-modified relationship between immunosuppression and viremia and atherogenic cholesterol patterns. These findings may contribute to our understanding of the high risk of dyslipidemia observed among persons aging with HIV. [ABSTRACT FROM AUTHOR]