Improved Survival Among all Interferon-α-Treated Patients in HCV-002, a Veterans Affairs Hepatitis C Cohort of 2211 Patients, Despite Increased Cirrhosis Among Nonresponders.

Background: As the era of interferon-alpha (IFN)-based therapy for hepatitis C ends, long-term treatment outcomes are now being evaluated.

Aim: To more fully understand the natural history of hepatitis C infection by following a multisite cohort of patients.

Methods: Patients with chronic HCV were prospectively enrolled in 1999-2000 from 11 VA medical centers and followed through retrospective medical record review.

Characterization of a peptide domain within the GB virus C NS5A phosphoprotein that inhibits HIV replication.

Background: GBV-C infection is associated with prolonged survival in HIV-infected people and GBV-C inhibits HIV replication in co-infection models. Expression of the GBV-C nonstructural phosphoprotein 5A (NS5A) decreases surface levels of the HIV co-receptor CXCR4, induces the release of SDF-1 and inhibits HIV replication in Jurkat CD4+ T cell lines.

Methodology/principal Findings: Jurkat cell lines stably expressing NS5A protein and peptides were generated and HIV replication in these cell lines assessed.

Effect of antiretroviral therapy and hepatitis c co-infection on changes in lipid levels in HIV-Infected patients 48 weeks after initiation of therapy.

Hepatitis C virus (HCV) commonly co-infects HIV-infected individuals. Antiretroviral therapy (ART) is associated with elevated serum lipid levels, and HCV infection is associated with low serum lipid levels. Fasting lipid levels were investigated in 1,434 ART-naïve HIV-infected people participating in the AIDS Clinical Trials Group (ACTG) Longitudinal Linked Randomized Trials (ALLRT) protocol who prospectively initiated ART with 3 agents.

Expression of GB virus C NS5A protein from genotypes 1, 2, 3 and 5 and a 30 aa NS5A fragment inhibit human immunodeficiency virus type 1 replication in a CD4+ T-lymphocyte cell line.

GB virus type C (GBV-C) is a common human flavivirus that has been associated with prolonged survival in HIV-positive individuals in several, though not all, epidemiological studies. There are five distinct GBV-C genotypes that are geographically localized, and it has been speculated that GBV-C genotypic differences may explain variable outcomes observed in different clinical studies. Expression of an 85 aa fragment of the GBV-C NS5A phosphoprotein (genotype 2) in a CD4+ T cell line (Jurkat) resulted in inhibition of HIV replication, mediated in part by decreased surface expression of the HIV coreceptor CXCR4 and upregulation of SDF-1.

The GBV-C envelope glycoprotein E2 does not interact specifically with CD81.

The addition of GB virus C (GBV-C) E2 protein to cells inhibits HIV replication in vitro, presumably triggered by interactions with a specific cellular receptor. Indirect evidence suggests that CD81 is the GBV-C E2 cellular receptor. We found that E2 binding to cells was not dependent upon human CD81, and that soluble CD81 did not compete with GBV-C E2 for cell binding.