The prevalence of metabolic syndrome is high among HIV-infected persons, but not higher than the prevalence among HIV-uninfected persons. Traditional risk factors play a more significant role in the development of metabolic syndrome than do HIV treatment-associated factors.

No abstract

Depression is a common comorbidity among HIV-infected individuals. We studied the relationship between depressive symptoms, risk behaviors (risky-sexual behavior, tobacco, alcohol and illicit drug use) and HIV outcomes. This cross-sectional study conducted in 2009 at Washington University HIV Clinic included screening for depression with patient health questionnaire (PHQ-9), survey of sexual behavior, illicit drug, alcohol and tobacco use within 30 days. Sociodemographics, plasma HIV RNA levels, CD4 cell counts and sexually transmitted disease (STD) test results were obtained from medical records. Multivariate logistic and linear regression models were used to assess the association between depressive symptoms severity and risk behaviors, HIV outcomes and combination antiretroviral therapy (cART) adherence. A total of 624 persons completed the assessment, of whom 432 (69%) were male and 426 (68%) African American. The median CD4 cell count was 410 cells/mm3 and 479 (77%) were on cART of whom 112 (23%) had HIV RNA level > 400 copies/mL. Overall, 96 (15%) had symptoms of major depressive disorder. Depressive symptom severity was associated with increased likelihood of high-risk drinking (Odds Ratio (OR), 2.4; 95% Confidence Interval (CI), 1.1–5.1), current tobacco use (OR, 1.8; 95%CI, 1.1–2.9), illicit drug use (OR, 1.7; 95%CI, 1.0–2.8) and risky-sexual behavior (OR, 1.5; 95%CI, 0.8–2.7). Sub-optimal cART adherence (visual analogue scale < 95%) was also associated with depressive symptoms severity (p< 0.05). After adjustment for age, sex, race, receipt of cART and cART adherence, depressive symptoms severity was independently associated with lower CD4 cell count (p< 0.05) but not with higher HIV RNA level (p= 0.39). Depression adversely affects HIV-infected individuals, requiring greater effort at utilizing multidisciplinary interventions.

Trends in transmitted drug resistance-associated mutations (TDRM) in HIV-1infection vary depending on geographic and cohort characteristics. The impact of TDRM among patients receiving fully active combination antiretroviral therapy (cART) is poorly characterized. This was a retrospective study of 801 HIV-1-infected treatment-naive patients from 2001 to 2009 who had pre-cART genotype resistance test results available. The prevalence of TDRM was compared for each year strata. Multivariate Cox proportional hazards regression models were used to assess factors associated with virologic failure at 48 weeks. TDRM was detected in 136 (17%) patients with ‡ 2 class TDRM in 20 patients. K103N/S was the most frequent (n = 77). There were no changes in the prevalence of mutations over time (P trend = 0.67). Six hundred and eleven patients were started on cART. Virologic failure occurred in 38% of those with TDRM and 24% of those without ( p < 0.01). In multivariate analysis, nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance was associated with a 1.5-fold increased risk of virologic failure. TDRM remains common among treatment-naive HIV-1-infected patients, affecting one in six patients. Transmission of NNRTI drug resistance was associated with risk of virologic failure despite initiation of genotype-guided cART.

To differentiate between the effects that antiretroviral drugs have on the endothelium and the secondary effects that they have on immune function, viral load, and dyslipidemia, 6 non-human immunodeficiency virus-infected human subjects were treated with lopinavir-ritonavir for 1 month and, on the basis of forearm blood flow, the treatment's effects on endothelial cell function were measured. Surprisingly, after exposure to lopinavir-ritonavir, absolute forearm blood-flow responses to the endothelium-dependent vasodilator, acetylcholine, increased significantly (P=.03), and forearm blood flow decreased to a greater extent during specific inhibition of NO synthase by N(G)-monomethyl-L-arginine. Thus, in this small cohort of subjects, short-term treatment with lopinavir-ritonavir does not appear to directly promote endothelial cell dysfunction.

No abstract

No abstract

A total of 192 HIV-1-infected antiretroviral-naive individuals had genotyping performed in our midwest university clinic between 2003 and 2005. The overall prevalence of resistance with either a reverse transcriptase or major protease mutation was 18%. There did not seem to be a significant difference in primary resistance patterns between different modes of HIV transmission (heterosexual versus men who have sex with men), gender or between white and African-American individuals.