HBV and HIV viral load but not microbial translocation or immune activation are associated with liver fibrosis among patients in South Africa

• Published in: BMC infectious diseases 2018-05, Vol.18 (1), p.214-214, Article 214
• Main Authors: Maponga, Tongai Gibson, Andersson, Monique I, van Rensburg, Christoffel J, Arends, Joop E, Taljaard, Jantjie, Preiser, Wolfgang, Glashoff, Richard H
• Format: Article
• Language: English
• Subjects: Adult; Anti-retroviral treatment; Antiretroviral agents; Antiretroviral Therapy, Highly Active; Biomarkers - blood; Care and treatment; CD4-Positive T-Lymphocytes - virology; Coinfection - virology; Cytokines; Development and progression; Dosage and administration; Elasticity Imaging Techniques; Female; Fibrosis; Health aspects; Hepatitis B; Hepatitis B - complications; Hepatitis B - immunology; Hepatitis B - virology; Hepatitis B infection; HIV; HIV Infections - complications; HIV Infections - drug therapy; HIV Infections - immunology; HIV Infections - virology; HIV patients; Humans; Lipopolysaccharide Receptors - blood; Liver Cirrhosis - diagnostic imaging; Liver Cirrhosis - immunology; Liver Cirrhosis - virology; Male; Middle Aged; South Africa; Tenofovir - therapeutic use; Transient elastography; Viraemia; Viral Load; Virus replication
• ISSN: 1471-2334; 1471-2334
• DOI: 10.1186/s12879-018-3115-8

Co-infection with HIV negatively impacts the progression of chronic hepatitis B virus (HBV) infection, including causing rapid progression to liver fibrosis. Sub-Saharan Africa represents arguably the most important intersection of high endemicity of both chronic hepatitis B virus (HBV) infection and HIV infection. We recruited 46 HBV/HIV-co-infected; 47 HBV-monoinfected; 39 HIV-monoinfected; and 37 HBV/HIV-uninfected patients from Tygerberg Hospital, Cape Town, South Africa. All HIV-infected patients were on antiretroviral therapy for ≥3 months. Liver stiffness measurements were assessed using the Fibroscan (Fibroscan 402, Echosens). Cell-based immunomarkers were measured by flow cytometry. Soluble serum/plasma immunomarkers were measured by Luminex technology and enzyme immunoassays. HIV (COBAS/Ampliprep TaqMan HIV-1) and HBV viral loads (in-house assay) were also performed. HBV/HIV co-infected patients showed significantly higher levels of immune activation %CD8+/HLA-DR+/CD38+ (median 30%, interquartile range: 17-53) and %CD8+/PD-1 (median 22%, interquartile range: 15-33), p ≤ 0.01 compared to all other study groups. Despite this, the HBV-mono-infected group had the highest proportion of patients with advanced liver fibrosis (≥13 kPa) as measured by Fibroscan (18%). HBV mono-infected patients showed highest expression of most cytokines including IL-17 and basic fibroblastic growth factor. There was significant positive correlation between detectable HIV and HBV viral replication and liver fibrosis but not immune activation or gut translocation. Highly-active antiretroviral therapy, including tenofovir, is effective against both HIV and HBV. Earlier therapy in the co-infected patients may therefore have controlled viral replication leading to better fibrosis scores when compared to HBV mono-infection in this study. On-going HBV and HIV viraemia, rather than microbial translocation or immune activation, appear to be the drivers of liver fibrosis. Moderate to advanced liver fibrosis in HBV-mono-infection may well indicate poor access to screening and treatment of HBV infection.