Research

Changes in viral load and HBsAg and HBeAg status with age in HBV chronic carriers in The Gambia

Maimuna E Mendy¹ , Samuel J McConkey^1,2 , Marianne AB Sande van der^1,3 , Sarah Crozier^1,4 , Steve Kaye^1,5 , David Jeffries¹ , Andrew J Hall⁶ and Hilton C Whittle¹

¹Medical Research Council Laboratories, Atlantic Boulevard, PO Box 273, Banjul, The Gambia

²Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland

³National Institute for Public Health and the Environment, Bilthoven, The Netherlands

⁴Medical Research Council Epidemiology Resource Centre, University of Southampton, Southampton, UK

⁵Imperial College, London, UK

⁶London School of Hygiene and Tropical Medicine, Keppel Street, London, UK

author email corresponding author email

Virology Journal 2008, 5:49doi:10.1186/1743-422X-5-49

Published:	16 April 2008

Abstract

Background

Little is known about changes in hepatitis B viral load (HBV DNA) in relation to age in Africa. The aim of this study is to determine the natural course of HBV chronic infection, particularly in relation to sequential changes in serum HBV DNA levels and hepatitis B surface (HBsAg) antigen/hepatitis e antigen (HBeAg) status by age.

Methods

The study was conducted on 190 HBV chronic carriers, aged 1–19 years who were followed for 19 years. 160, 99 and 123 were traced at 5, 9 and 19 years later. All available samples were tested for HBsAg and HBeAg, whilst 170, 61, 63 and 81 were tested for HBV DNA at the baseline, and at 5, 9 and 19 years following recruitment.

Results

In general HBeAg which correlated with high levels of HBV DNA was lost at a much faster rate than HBsAg. 86% of the carriers who were recruited at the age of 1–4 yrs lost HBeAg by the age of 19 years compared to 30% who lost HBsAg. HBeAg negative carriers had serum HBV DNA levels of < 10⁵ copies per mL, HBV DNA positivity declined from 100% in 1–4 yrs old carriers at recruitment to 62.5%,60% and 88% at 5, 9 and 19 years respectively following recruitment.

Conclusion

After 19 years of follow up, the majority of HBV surface antigen carriers had lost HBeAg positivity and had low levels of viral replication. However small proportions (10–20%) retained HBeAg and continue to have high levels of viral replication.