The implications of high levels of hepatitis B and HIV coinfection (HBV) are being ignored by HIV treatment programmes in sub-Saharan Africa, according to a review article published in the September edition of Liver International.
The lifetime risk of HBV infection in Africa is estimated to be 60%. Acquisition from other children during childhood is the most common route of transmission, with infants and young children more likely than adults to become chronic carriers capable of infecting others.
It is estimated that there are 50 million chronic carriers in Africa, and an estimated 12.5 million deaths will occur from liver disease within this population as a result of HBV (230,000 deaths per year).
Rates of surface antigen carriage vary from 9% in South Africa to 20% in the Democratic Republic of Congo. There is also considerable variation between rural and urban settings within countries: in South Africa, for example, the predominantly rural Eastern Cape reports a prevalence of 15.5%, compared with 1.3% in the township of Soweto. Worldwide, hepatitis B is more common in men than in women, despite little difference in levels of exposure. In Africa the male: female prevalence ratio varies from 1.5:1 to 4:1.
Evidence suggests a higher rate of infectious carriage of HBV in HIV-positive individuals in the Democratic Republic of Congo and Zambia, although smaller studies from earlier stages of the HIV epidemic do not report the same association. No difference in the overall prevalence of HBV has been observed in HIV-positive people compared to HIV-negative people in Africa, the authors note, in contrast to findings in the United States.
The high rate of HIV/HBV coinfection has implications for treatment programmes designed to expand access to antiretroviral treatment, the authors say. There is an increased risk of death from liver disease in HIV/HBV coinfected people, and a higher risk of hepatotoxicity associated with certain drugs used in G+HIV and AIDS treatment.
Another problem is the possibility of reactivation of HBV as a result of increasing immunologic pressure on the virus, which is a result of immune reconstitution driven by antiretroviral treatment. This reactivation has been noted even when 3TC (lamivudine, Epivir) is included in the HIV treatment regimen, and without the development of lamivudine resistance in HBV. However its frequency is poorly characterised and the observation is based on case reports only, so it is unclear to what extent this problem will manifest in African populations.
There are also implications for lamivudine use. Lamivudine is one of the few anti-HIV drugs that is also active against HBV, and some guidelines recommend that where limited options exist for coinfected patients, the drug should be reserved for HBeAg-positive patients with clinical hepatitis in order to reduce risk of HBV evolving lamivudine resistance. However 3TC is included in all first-line antiretroviral regimens, leading to the risk of lamivudine-resistant HBV.
Finally, response to HBV vaccination in HIV-positive people is uncertain, particularly in small children infected with HIV who are primary targets for vaccination campaigns throughout Africa.
The authors say that surveillance and research of HBV needs to be stepped up in sub-Saharan Africa in order to understand better the interaction between the two viruses.
Burnett RJ et al. Hepatitis B virus and human immunodeficiency virus co-infection in sub-Saharan Africa: a call for further investigation. Liver International 25: 201-213, 2005.