Triple burden at the HIV–hepatitis B–malaria interface: viral–parasite interactions, epidemiological complexity and the case for integrated surveillance and community-based prevention in sub-Saharan Africa

Human immunodeficiency virus (HIV), hepatitis B virus (HBV) and malaria overlap across sub-Saharan Africa, yet they differ in how they spread, how long they last and how programmes measure success. This critical narrative review examines the evidence for biological interaction at each interface, the diagnostic and epidemiological traps that their overlap creates, and the case for integrated surveillance and community prevention. HIV-associated immunosuppression consistently increases the frequency and severity of malaria, and acute malaria transiently raises plasma HIV RNA. HIV accelerates the natural history of chronic HBV. Because HIV treatment and prevention are shifting towards regimens and long-acting products with no activity against HBV, a documented hepatitis B surface antigen result has become essential before any regimen change. Antiretroviral and antimalarial drugs also interact in clinically relevant ways. A direct interaction between HBV and Plasmodium is plausible, through interferon-mediated suppression of HBV during malaria, but it rests mainly on animal models and small, inconsistent human studies, and no reliable estimate of triple infection exists. Fever, anaemia and abnormal liver tests during malaria can mask a concurrent chronic viral infection, and routine facility data can produce apparent coinfection patterns that reflect testing intensity rather than biology. Drawing on the World Health Organization’s guidance on integrated disease surveillance and response, we describe a detect–verify–act approach that links community signals, confirmatory testing and confidential longitudinal records, while each infection keeps its own indicators and review cycle. Integration should rest on shared delivery, not on assumed shared pathogenesis, and prospective cohorts and implementation trials are needed to show whether it improves outcomes and equity.

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Publication Details

Journal
F1000Research
Published
2026-11-11
DOI
https://doi.org/10.12688/f1000research.193683.1
Primary Topic
HIV/AIDS Research and Interventions
Type
article
Field-Weighted Citation Impact
0.00
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article

Triple burden at the HIV–hepatitis B–malaria interface: viral–parasite interactions, epidemiological complexity and the case for integrated surveillance and community-based prevention in sub-Saharan Africa

Matthew Chibunna Igwe, G. A. Nwankwo, Ogbonna Alphonsus Ogbuabor, Oluchi Jacinta Ossai
F1000Research
HIV/AIDS Research and Interventions
article

Triple burden at the HIV–hepatitis B–malaria interface: viral–parasite interactions, epidemiological complexity and the case for integrated surveillance and community-based prevention in sub-Saharan Africa

Matthew Chibunna Igwe, G. A. Nwankwo, Ogbonna Alphonsus Ogbuabor, Oluchi Jacinta Ossai
article en

Abstract

Human immunodeficiency virus (HIV), hepatitis B virus (HBV) and malaria overlap across sub-Saharan Africa, yet they differ in how they spread, how long they last and how programmes measure success. This critical narrative review examines the evidence for biological interaction at each interface, the diagnostic and epidemiological traps that their overlap creates, and the case for integrated surveillance and community prevention. HIV-associated immunosuppression consistently increases the frequency and severity of malaria, and acute malaria transiently raises plasma HIV RNA. HIV accelerates the natural history of chronic HBV. Because HIV treatment and prevention are shifting towards regimens and long-acting products with no activity against HBV, a documented hepatitis B surface antigen result has become essential before any regimen change. Antiretroviral and antimalarial drugs also interact in clinically relevant ways. A direct interaction between HBV and Plasmodium is plausible, through interferon-mediated suppression of HBV during malaria, but it rests mainly on animal models and small, inconsistent human studies, and no reliable estimate of triple infection exists. Fever, anaemia and abnormal liver tests during malaria can mask a concurrent chronic viral infection, and routine facility data can produce apparent coinfection patterns that reflect testing intensity rather than biology. Drawing on the World Health Organization’s guidance on integrated disease surveillance and response, we describe a detect–verify–act approach that links community signals, confirmatory testing and confidential longitudinal records, while each infection keeps its own indicators and review cycle. Integration should rest on shared delivery, not on assumed shared pathogenesis, and prospective cohorts and implementation trials are needed to show whether it improves outcomes and equity.

F1000ResearchVol. 15
Kampala International University (UG), Ignatius Ajuru University of Education (NG)
HIV/AIDS Research and Interventions
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