The Essential Need for Trust When Transmission Risk Cannot Be Eliminated in HIV-Remission Trials.

Analytic treatment interruption (ATI) is scientifically necessary in HIV-remission ("cure") studies to test the effects of new interventions. However, stopping antiretroviral treatment poses risks to research participants and their sexual partners. Ethical debate about whether and how to conduct such studies has largely centered on designing risk-mitigation strategies and identifying the responsibilities of research stakeholders. In this paper, we argue that because the possibility of HIV transmission from research participants to partners during ATI cannot practicably be eliminated-that is, it is ineliminable-the successful conduct of such trials ultimately depends on relationships of trust and trustworthiness. We describe our experiences with conducting and studying HIV-remission trials with ATI in Thailand to examine the strengths, complexities, and limitations of the risk-mitigation and responsibility approaches and to explore ways in which the building of trust-and trustworthiness-may help enhance the scientific, practical, and ethical dimensions of these trials.

Viral Blips After Treatment Initiation During Acute Human Immunodeficiency Virus Infection.

Transient viral blips ≥20 copies/mL were observed in 16.9% of acutely treated adults with HIV. Blip incidence increased from 0.0 (95% CI, 0.0-2.9)/100 person-years after ART in Fiebig I to 15.9 (7.6-29.2) in Fiebig V. Increasing viral load and Fiebig stage at ART initiation were independently predictive of blips.

The immunogenicity and safety of pneumococcal conjugate vaccine in human immunodeficiency virus-infected Thai children.

BACKGROUND: HIV-infected children have high risk of invasive pneumococcal disease (IPD) despite receiving highly active antiretroviral therapy (HAART). This study aimed to determine the immunogenicity and safety of a 7-valent pneumococcal conjugate vaccine (PCV-7) in Thai HIV-infected children compared to HIV-exposed uninfected children. METHODS: A prospective study was conducted among children 2 months to 9 years. The number of PCV-7 doses depended upon age and HIV status; 2-6 months of age: 3 doses; 7-23 months of age: 2 doses; HIV-infected child ≥24 months: 2 doses and HIV-exposed child ≥24 months: 1 dose. Serotype-specific pneumococcal IgG antibody concentrations were measured at baseline and 28 days after complete vaccination. The primary end point was the proportion of children who achieved serotype-specific IgG antibody concentration at a cut off level ≥0.35 µg/mL. Secondary end points were a 4-fold increase in serotype-specific IgG antibody, rates of adverse events and predictors for seroconversion among HIV-infected children. RESULTS: Fifty-nine HIV-infected and 30 HIV-exposed children were enrolled. The median (IQR) age was 97 (67-111) and 61 months (51-73), respectively (p<0.001). Among HIV-infected children, current and nadir CD4 counts were 1,079 cell/mm(3) and 461 cell/mm(3), respectively. The proportion of children who achieved pneumococcal IgG ≥0.35 µg/mL was in the range of 85-98% in HIV-infected and 83-100% in HIV-exposed children depending on serotype. The lowest response was to serotype 6B in both groups. The 4-fold increase in serotype-specific IgG concentrations was similar between HIV-infected and HIV-exposed groups, except for serotype 9V (p=0.027). HIV-infected children who had a history of AIDS had a lower antibody response to serotype 23F (p=0.025). Seven (12%) HIV-infected children had a grade 3 local reaction. CONCLUSION: PCV-7 is highly immunogenic and safe among HIV-infected children treated with HAART. The use of the pneumococcal conjugate vaccine among HIV-infected children is encouraged in order to prevent IPD.

Henoch-Schönlein purpura and thrombocytopenia after planned antiretroviral treatment interruption in a Thai girl with HIV infection.

A handful of Henoch-Schönlein purpura (HSP) cases have been reported in HIV-infected adult patients. We report herein the case of an 11-year-old Thai girl with HIV infection, who developed severe abdominal pain and palpable purpura consistent with HSP, 3 months after planned antiretroviral treatment interruption (PTI). One month later she developed thrombocytopenia. It is possible that an HIV effect on vascular endothelium or PTI-associated immune activation contributed to HSP and thrombocytopenia.