AIDS-defining events and deaths in HIV-infected children and adolescents on antiretrovirals: a 14-year study in Thailand

BACKGROUND: Data are scarce on the long-term clinical outcomes of perinatally HIV-infected children and adolescents receiving antiretroviral therapy (ART) in low/middle-income countries. We assessed the incidence of mortality before (early) and after (late) 6-month of ART and of the composite outcome of new/recurrent AIDS-defining-event or death >6 months after ART start (late AIDS/death) and their associated factors. METHODS: Study population was perinatally HIV-infected children (≤18 years) initiating ART within the Program for HIV Prevention and Treatment observational cohort (NCT00433030). Factors associated with late AIDS/death were assessed using competing risk regression models accounting for loss-to-follow-up, and included baseline and time-updated variables. RESULTS: Among 619 children, "early" mortality incidence was 99 deaths per 1000-PYFU (95%CI; 69-142) and "late" mortality 6 per 1000-PYFU (95%CI; 4-9). Of the 553 children alive >6 months after ART initiation, median age at ART initiation was 6.4 years, CD4% 8.2% and HIV-RNA 5.1 log10 copies/mL. 38 (7%) children developed late AIDS/death after median time of 3.3 years: 24 died and 24 experienced new/recurrent AIDS-defining-events (10 subsequently died). Factors independently associated with late AIDS/death were: current age ≥13 years (adjusted sub-distribution hazard-ratio 4.9; 95%CI; 2.4-10.1), HIV-RNA always ≥400 copies/mL (12.3; 4.0-37.6), BMI-z-score always <-2 SD (13.7; 3.4-55.7), and hemoglobin <8g/dL at least once (4.6; 2.0-10.5). CONCLUSIONS: After the initial 6 months of ART, being an adolescent, persistent viremia, poor nutritional status and severe anemia were associated with poor clinical outcomes. This supports the need for novel interventions that target children, particularly adolescents with poor growth and uncontrolled viremia

Human immunodeficiency virus-hepatitis C virus co-infection in pregnant women and perinatal transmission to infants in Thailand

Objectives: The objectives of this study were to assess the prevalence and factors associated with hepatitis C virus (HCV) infection in human immunodeficiency virus (HIV)-infected and -uninfected Thai pregnant women and the rate of HCV transmission to their infants. Patients and methods: Study subjects included 1435 HIV-infected pregnant women and their infants, enrolled in a perinatal HIV prevention trial, and a control group of 448 HIV-uninfected pregnant women. Women were screened for HCV antibodies with an enzyme immunoassay. Positive results were confirmed by recombinant immunoblot and HCV RNA quantification. Infants were tested for HCV antibodies at 18 months or for HCV RNA at between 6 weeks and 6 months. Results: Of the HIV-infected women, 2.9% were HCV-infected compared to 0.5% of HIV-uninfected women (p = 0.001). Only history of intravenous drug use was associated with HCV infection in HIV-infected women. Ten percent of infants born to co-infected mothers acquired HCV. The risk of transmission was associated with a high maternal HCV RNA (p = 0.012), but not with HIV-1 load or CD4 count. Conclusions: Acquisition of HCV through intravenous drug use partially explains the higher rate of HCV infection in HIV-infected Thai women than in HIV-uninfected controls. Perinatal transmission occurred in 10% of infants of HIV-HCV-co-infected mothers and was associated with high maternal HCV RNA

The interrelated transmission of HIV-1 and cytomegalovirus during gestation and delivery in the offspring of HIV-infected mothers

Our objective was to analyze, in formula-fed infants, correlates of HIV mother-to-child transmission, including cytomegalovirus (CMV) infection. HIV-infected infants were matched with HIV uninfected by maternal HIV RNA in a case-control design. Infant CMV infection was determined by CMV IgG at 18 months and timed by earlier CMV IgM or CMV DNA. Correlations were assessed using logistic regression. In utero HIV infection was independently associated with congenital CMV infection (P - 0.01), intrapartum HIV infection with congenital-plus-intrapartum/neonatal CMV infection (P = 0.01), and overall HIV with overall CMV infection (P = 0.001), and prematurity (P = 0.004). Congenital and acquired CMV infections are strong independent correlates of mother-to-child HIV transmission