Down-regulation of intra-hepatic T-cell signaling associated with GB virus C in a HCV/HIV co-infected group with reduced liver disease.

Background & Aims: Studies have shown that GB virus C (GBV-C) infection leads to reduced liver disease in hepatitis C virus (HCV)/human immunodeficiency virus (HIV) co-infection. Considering that the underlying mechanism(s) are unknown, we aim to identify differential gene and protein expression associated with GBV-C in HCV/HIV co-infection that may be responsible for reduced liver disease.

Methods: Liver, peripheral blood mononuclear cells (PBMCs), and plasma samples were collected from 43 HCV/HIV patients.

GB virus C genotype 2 predominance in a hepatitis C virus/HIV infected population associated with reduced liver disease.

Background And Aim: GB virus C (GBV-C) infection in hepatitis C virus (HCV)/HIV co-infection is associated with a significant reduction in the severity of HCV-related liver disease. The role of GBV-C genotype in this association is unknown. It has been suggested that GBV-C genotype may influence CD4 positive T-cell counts in HCV/HIV co-infected patients.

Differential expression of the CXCR3 ligands in chronic hepatitis C virus (HCV) infection and their modulation by HCV in vitro.

To investigate chemokine expression networks in chronic hepatitis C virus (HCV) infection, we used microarray analysis to determine chemokine expression in human infection and in chimpanzees experimentally infected with HCV. The CXCR3 chemokine family was highly expressed in both human and chimpanzee infection. CXCL10 was the only CXCR3 chemokine elevated in the serum, suggesting that it may neutralize any CXCR3 chemokine gradient established between the periphery and liver by CXCL11 and CXCL9.

Reduction in hepatitis C-related liver disease associated with GB virus C in human immunodeficiency virus coinfection.

Background & Aims: It has been reported that GB virus C infection (GBV-C) leads to improved morbidity and mortality in patients with human immunodeficiency virus (HIV) infection. However, GBV-C has no effect on the course of liver disease in hepatitis C virus (HCV) monoinfection. The aim of the study was to determine the influence of GBV-C infection on liver disease in patients with HCV/HIV coinfection.

Chronic hepatitis C virus infection: genotyping and its clinical role.

Chronic hepatitis C virus (HCV) infection is a worldwide public health problem with a global prevalence of 2%. A high proportion of those infected are at risk of developing cirrhosis and hepatocellular carcinoma and modeling data predicts that the burden of disease could soon increase substantially. The liver disease associated with chronic infection has led investigators to look for correlates between viral properties and disease progression, severity of disease and the response to antiviral therapy.

Genomics of hepatitis B and C infections: diagnostic and therapeutic applications of microarray profiling.

Microarray profiling offers many potential advances in diagnostic and therapeutic intervention in human disease because of its unparalleled ability to conduct high-throughput analysis of gene expression. However, limitations of this technique relate in part to issues regarding the various methodologies and experimental designs as well as difficulties in the interpretation of results. Despite this, microarray profiling has led to a better understanding of the molecular pathogenesis of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection.

GB virus C: insights into co-infection.

GB virus C (GBV-C) is a single stranded positive sense RNA virus, which is a member of the Flaviviridae. It has a close sequence homology and genomic organisation to hepatitis C virus (HCV). However, unlike HCV it is not hepatotrophic.

Male to male sex is associated with a high prevalence of exposure to GB virus C.

Co-infection with GB virus C (GBV-C) and human immunodeficiency virus (HIV) appears to reduce mortality for HIV/AIDS. Epidemiological and demographic factors for GBV-C were examined prospectively in 167 subjects at risk for co-infection. We attempted to establish a hierarchical exposure risk for GBV-C.