The aim of this study was to determine the prevalence of hepatitis B virus (HBV) infection in a cohort of HIV-infected Rwandan children and adolescents on combination antiretroviral therapy (cART), and the success rate of HBV vaccination in those children found to be HBV negative.
HIV-infected children and adolescents (age 8–17 years) receiving cART with CD4 T-cells count ≥200 cells/mm3 and/or ≥15% and without prior HBV vaccination (by history, vaccination cards and clinic records) underwent serologic testing for past (negative HBV surface antigen [HBsAg] with positive antibody to HBV core antigen [cAb] and to HBsAg [anti-HBs]) or active HBV infection (positive HBsAg). Children with any positive HBV serologic tests were excluded from further vaccination; all others completed 3 HBV immunizations with 10 µg of ENGERIX-B. Anti-HBs titer was measured 4–6 weeks after the last immunization.
Of 88 children, 6 (7%) children had active HBV infection and 8 (9%) had past HBV infection. The median (interquartile range) age, CD4 T-cell count and cART duration were 12.3 (10.1–13.9) years, 626 (503 to 942) cells/mm3 and 1.9 (1.5–2.7) years, respectively. Seventeen children had detectable plasma HIV-1 RNA. Seventy-3 children completed 3 immunizations with median (interquartile range) postimmunization anti-HBs concentration of 151 mIU/mL (1.03–650). Overall, 52 children (71%, 95% confidence interval: 61–82) developed a protective anti-HBs response. HIV-1 RNA and CD4 T-cell count were independent predictors of a protective anti-HBs response. Protective anti-HBs response was achieved in 82% of children with undetectable HIV-1 RNA and 77% with CD4 T cells ≥350/mm3.
The substantial HBV prevalence in this cohort suggests that HIV-infected Rwandan children should be screened for HBV before cART initiation. HIV viral suppression and CD4 T cells ≥350/mm3 favored the likelihood of a protective response after HBV vaccination.Key Words: Hepatitis B, HIV-infected children and adolescents, Rwanda.
From the *Department of Pediatrics, Kigali University Teaching Hospital, Kigali, Rwanda; †Department of Global Health, Academic Medical Center, Amsterdam Institute for Global Health and Development; ‡Royal Tropical Institute (KIT), Biomedical Research, Epidemiology Unit, Amsterdam, The Netherlands; §National Reference Laboratory, Kigali, Rwanda; ¶Treatment and Research on HIV/AIDS Centre (TRAC-plus), Outpatients clinic, Kigali, Rwanda; and ‖Utrecht University Children’s Hospital, University Medical Centre of Utrecht, Utrecht, The Netherlands.
Accepted for publication August 28, 2012.
This study was funded by the Netherlands–African partnership for capacity development and clinical interventions against poverty-related diseases (NACCAP). The authors have no other funding or conflicts of interest to disclose.
Some data were presented at 19th Conference on Retroviruses and Opportunistic Infections, Seattle, WA, March 5–8, 2012.
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Address for correspondence: Philippe R. Mutwa, MD, INTERACT Rwanda, PO Box: 655, Kigali, Rwanda. E-mail: firstname.lastname@example.org.