Results: Thirty-five HIV+ subjects and 37 controls were included in the analysis. Among HIV+ subjects, the median age was 10 years, body mass index was 18.7 kg/m(2), 37% were male, CD4 count was 32%, 77% had HIV-RNA <400 copies/mL, and 86% were on antiretrovirals. At baseline, HIV+ had higher lipids and C-reactive protein. HIV-infected had higher internal carotid this website artery (ICA) and common carotid artery (CCA) IMT (mm) (ICA: HIV+, 0.90; controls,

0.78 [P = 0.01]; CCA: HIV+, 1.00; controls, 0.95 [P = 0.05]). At 48 weeks, CD4% increased and low-density lipoprotein decreased in HIV-infected subjects. ICA and CCA median changes for HIV-infected subjects were -0.23 and -0.15 mm, respectively (both P < 0.01). In controls, only CCA changed (P = 0.04). Between-group changes were not significant, except when only 31 perinatally infected HIV+ subjects and the controls were compared (CCA P = 0.04). In multiple regression analyses of HIV+ subjects, antiretroviral therapy duration and CD4% were associated with cIMT changes.

Conclusions: Higher cIMT was found eFT-508 purchase in HIV-infected subjects than in healthy controls, but at 48 weeks, cIMT was similar between groups. These data suggest that HIV-infected children/young adults are at high risk of CVD, but lipid control, immune restoration, and viral suppression with continuous antiretroviral therapy may prevent

its worsening.”
“The concurrent detection of hepatitis

B e antigen (HBeAg) and its corresponding antibody (anti-HBe) in patients with chronic hepatitis B virus (HBV) infection is well established but the clinical features remain poorly understood. Demographic information, clinical and laboratory data were collected from 1624 consecutive inpatient records of patients with chronic hepatitis Fedratinib mw B. Viral genotype, basic core promoter and precore mutations were determined by direct sequencing. In vitro HBeAg and anti-HBe binding experiments were conducted with three pairs of HBeAg-positive and anti-HBe-positive serum samples, which were mixed at variable ratios and incubated at 37 degrees C for 3-24 h. Of the 1624 chronic patients, 169 (10.4%) had concurrent HBeAg and anti-HBe positivity, and this was associated with intermediate age and HBV-DNA load, higher alanine aminotransferase level and more pronounced liver damage compared with HBeAg-positive or anti-HBe-positive patients alone. HBeAg and anti-HBe titres (median and interquartile range, S/CO) in the concurrent positive group were 4.2 (1.89.6) and 0.54 (0.27-0.72), which were closer to their respective cut-off values than those of HBeAg-positive or anti-HBe-positive groups alone. For the cases successfully sequenced, 110/134 (82.1%) harboured T1762/A1764 or/and A1896 mutants. The binding experiments showed that HBeAg and anti-HBe could be concurrently observed provided an optimal ratio (HBeAg to anti-HBe) was chosen.