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The article presents a randomized study which determines the factors that influence the virologic and immunologic outcome of structured interruptions (STIs) in HIV chronic infection. The main outcome measures of the study was aimed at testing the noninferiority of STIs to continuous highly active antiretroviral therapy (HAART) in terms of CD4 cell count. The results of the study is presented and discussed.

Since 1989, the emergence of resistant human immunodeficiency virus mutants has been documented for any new antiretroviral agent introduced in the clinical setting it is a major cause of failure of antiretroviral therapy that may ultimately compromise the antiretroviral's efficacy in the general population. In most cases, resistance is due to poor adherence by the patient and/or to low potency of the therapeutic regimen. Resistance is called "primary" if detected in treatment-naive persons and is called "acquired" when it develops in treatment- experienced persons. This latter population represents potential transmitters of resistant viruses to newly infected persons. Data about the actual prevalence of resistance are derived from studies that differ in design, sample size, geographic area, and definitions. For this reason, a limited number of surveillance programs have been established in the past, both in countries where highly active antiretroviral therapy is widely accessible and in geographic areas where it is being introduced. [ABSTRACT FROM AUTHOR]

Summary: Background: Microbial translocation from the gut lumen has been involved in the pathogenesis of liver damage in hepatitis C virus (HCV) infection. Aim: To investigate the impact of direct‐acting antiviral treatment on microbial translocation and T‐cell activation, in patients with hepatitis C‐related liver disease. Methods: We enrolled two groups of HCV‐infected patients undergoing direct‐acting antiviral treatment: patients with fibrosis ≥F3 according to Metavir (Group ≥F3); patients with hepatitis C recurrence after liver transplantation and Metavir ≥F2 (Group Liver Transplantation + ≥F2). All patients were treated with direct‐acting antivirals based on ongoing guidelines. Surrogate biomarkers of microbial translocation (plasma concentrations of soluble‐CD14, lipopolysaccharide‐binding protein and intestinal fatty acid‐binding protein) were evaluated at baseline, at first month, at the end of treatment and 3 months later. T‐cell activation was measured by expression of CD38+ HLA‐DR at the same time points, only in Group ≥F3. Results: There were 32 patients in Group ≥F3 and 13 in Group LT + ≥F2. At baseline, levels of soluble‐CD14 and lipopolysaccharide‐binding protein were significantly higher in both groups vs healthy controls. Baseline soluble‐CD14 correlated with glutamic‐oxalacetic transaminase (r = 0.384, P = 0.009) and glutamic‐pyruvic transaminase (r = 0.293, P = 0.05). A significant decrease in plasma levels of surrogate microbial translocation biomarkers was observed during and after treatment in the two groups although values were not normalised. In Group ≥F3, CD38+ HLADR+ T‐cell expression was significantly decreased by direct‐acting antiviral treatment. Relapsers (9%) showed higher soluble‐CD14 levels at baseline. Conclusion: Surrogate microbial translocation markers and T cell activation are increased in HCV‐infected patients with liver fibrosis and decrease during direct‐acting antiviral treatment. [ABSTRACT FROM AUTHOR]