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  • Open Access

Characterizing the epidemiology and interaction between HIV-1 and HBV co-infection in South Africa

  • 1, 2,
  • 3,
  • 4,
  • 5,
  • 4, 5,
  • 3 and
  • 1, 2, 6
BMC Infectious Diseases201414 (Suppl 2) :P18

https://doi.org/10.1186/1471-2334-14-S2-P18

  • Published:

Keywords

  • ELISpot Assay
  • Coinfection Rate
  • HBsAg Prevalence

Introduction

Anti-Retroviral Therapy (ART) has dramatically reduced morbidity and mortality associated with HIV/AIDS. However, this has left a niche for the emergence of liver disease in HIV-positive individuals co-infected with HBV. Despite the geographical overlap between highly endemic HBV and HIV in Southern Africa, there is a wide range in the prevalence of co-infection. We therefore set out to characterize the epidemiology of HIV/HBV co-infection in a Durban cohort, and to investigate the possible impact of HBV infection on HIV disease progression.

Materials and methods

We investigated a cohort of 498 adult women recruited via antenatal/postnatal clinics in Durban, South Africa, of whom 72 were HIV negative and 426 were chronically HIV-infected and ART-naïve (median CD4 count 368 cells/mm3, median HIV-1 RNA load 4.47 log10 copies/ml). We screened plasma for HBsAg by ELISA (Biokit). CD8+ T cell responses to HIV peptides were quantified by IFN-gamma ELISpot assay in 325 HIV-infected individuals including 35 with HBV coinfection.

Results

Overall HBsAg prevalence was 46/498 (9.2%; 95%-confidence interval 7-12%); coinfection rates were 9.4% in HIV-positive and 8.3% in HIV-negative individuals. CD4 counts were significantly lower in with HBV/HIV coinfection than with HIV monoinfection (302 vs. 375 cells/mm3; p=0.02). However, HBV status made no significant impact on HIV viral load (4.49 log10 copies/ml in coinfection vs. 4.46 log10 in monoinfection). There was no difference in breadth, magnitude, or protein-specificity of IFN-gamma responses to HIV according to HBV status.

Conclusions

In this cohort of Durban women, 9% were coinfected with HBV. Women with HIV/HBV co-infection had significantly lower CD4 counts, highlighting the potential detriment of coinfection. However, in a small subset we did not find a difference in CD8+ T cell responses to HIV. These data contribute towards an improved understanding of the scale of the HIV/HBV coinfection problem in Africa, and suggest that adverse outcomes are mediated by factors other than CD8+ T cell responses to HIV.

Authors’ Affiliations

(1)
Nuffield Department of Medicine, University of Oxford, Oxford, OX1 3SY, UK
(2)
Department of Infectious Diseases and Microbiology, Oxford University Hospitals, John Radcliffe Hospital, Headington, Oxford, OX3 9DU, UK
(3)
Institute of Infection & Global Health, University of Liverpool, Liverpool, L69 7BE, UK
(4)
Department of Pediatrics, University of Oxford, Peter Medawar Building, Oxford, OX1 3SY, UK
(5)
HIV Pathogenesis Program, Doris Duke Medical Research Institute, University of KwaZulu-Natal, Durban, South Africa
(6)
NIHR Biomedical Research Center, John Radcliffe Hospital, Headington, Oxford, OX3 9DU, UK

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