OA04-05. Safety and viral load changes in HIV-1 infected subjects treated with autologous dendritic immune therapy following ART discontinuation (CTN#239)

International audiencen.

Management and treatment of hepatitis C virus in patients with HIV and hepatitis C virus coinfection: A practical guide for health care professionals

Concomitant HIV and hepatitis C virus (HCV) is a common yet complex coinfection. The present document is a practical guide for treating HCV infection in people coinfected with HIV. Effective antiretroviral therapies have prolonged survival rates for HIV-infected people over the past decade, which have made latent complications of HCV major causes of morbidity and mortality in these patients. Advances in the treatment of HCV (eg, combined pegylated interferon and ribavirin) offer the possibility of eradicating HCV infection in coinfected persons. The treatment of HCV must be considered in all cases. Intensive management of the adverse effects of HCV treatment is one of the factors for the success of these therapies. HCV eradication is predicted to decrease the mortality associated with coinfection and reduce the toxicity of HIV treatment

Changes in Function of HIV-Specific T-Cell Responses with Increasing Time from Infection

Recently HIV-infected individuals have virus-specific responses characterized by IFN-γ/IL-2 secretion and proliferation rarely seen in chronic infection. To investigate the timing of loss of HIV-specific T-cell function, we screened cells from 59 treatment-naïve HIV-infected individuals with known dates of infection for proteome-wide responses secreting IFN-γ/IL-2 and IFN-γ alone by ELISPOT. HIV peptide-specific proliferation was assessed by carboxyfluorescein diacetate succinimidyl ester (CFSE) dilution. The contribution of IFN-γ/IL-2 and IFN-γ-only secretion to the total HIV-specific response was compared in subjects infected <6, 6–12, and 12–36 mo earlier. The frequency of IFN-γ/IL-2-secreting cells fell, while that of IFN-γ-only secretion rose with time from infection. HIV peptide-specific proliferative responses were almost exclusively mediated by CD8+ T cells, and were significantly lower in cells obtained from the 12–36 mo versus < 6 mo post-infection groups. By the second year of infection there was a significant difference in these functions compared to those assessed within 6 mo