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Last Updated: 07/06/2024
Clinical and immunopathological consequences of chronic HBV and Plasmodium falciparum co-infections (HEPMAL)
Objectives
To test the primary hypothesis that chronic HBV infections elicit a strong regulatory T cell environment that dampens induction of the needed pro-inflammatory response against liver stage malaria parasites.
Hepatitis B virus (HBV) and Plasmodium are very common pathogens in sub-Saharan Africa and sometimes occur as co-infections. Both pathogens infect liver cells and elicit pathogen-specific immune responses that may mediate both protection and immunopathology. HBV infection of the liver, even in an acute form, is usually long term, while Plasmodium liver infections are usually over a limited period after an infectious mosquito bite. Immune responses, especially against chronic HBV infections, can thus affect liver stage malaria-specific T cell responses. There is however no consensus on how HBV induced immune responses affect liver stage anti-malarial immunity. Plasmodium infection could also, in the reverse, contribute to liver pathology in chronic HBV-infected subjects. Malaria vaccine candidate trials usually exclude individuals infected with immune modulating pathogens such as HBV. However, vaccine induced responses could be compromised in HBV-infected persons if vaccines are later approved for routine immunization. Investigation of the potential impact of chronic HBV infection on malaria liver stage-specific immune response quality is therefore essential. We will recruit chronic HBV-infected subjects from the Gastroenterology Clinic of the Korle Bu Teaching Hospital in Accra and followed up once a month over one year. The study will provide useful data on the by-stander effects of chronic HBV infection on immunity and outcome of Plasmodium liver stage infections as well as the impact of liver stage Plasmodium infection on the clinical course of chronic HBV infection in co-infected individuals.
Aug 2020 — Jul 2024
$538,278