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

Background: 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. Methods: 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. Results: 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. Discussion: 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.

Description

CITATION: Maponga, T. G., et al. 2018. HBV and HIV viral load but not microbial translocation or immune activation are associated with liver fibrosis among patients in South Africa. BMC Infectious Diseases, 18:214, doi:10.1186/s12879-018-3115-8.
The original publication is available at https://bmcinfectdis.biomedcentral.com
Publication of this article was funded by the Stellenbosch University Open Access Fund.

Keywords

HIV infections, Hepatitis B, Cytokines, Antiretroviral agents, Liver -- Diseases

Citation

Maponga, T. G., et al. 2018. HBV and HIV viral load but not microbial translocation or immune activation are associated with liver fibrosis among patients in South Africa. BMC Infectious Diseases, 18:214, doi:10.1186/s12879-018-3115-8

URI

http://hdl.handle.net/10019.1/103993

Collections

Research Articles (Medical Virology)

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