hepatitis b virus infection does not significantly influence plasmodium parasite density in asymptomatic infections in ghanaian transfusion recipients乙型肝炎病毒感染不显著影响疟原虫的寄生虫密度在加纳的无症状感染输血.pdfVIP

hepatitis b virus infection does not significantly influence plasmodium parasite density in asymptomatic infections in ghanaian transfusion recipients乙型肝炎病毒感染不显著影响疟原虫的寄生虫密度在加纳的无症状感染输血.pdf

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hepatitis b virus infection does not significantly influence plasmodium parasite density in asymptomatic infections in ghanaian transfusion recipients乙型肝炎病毒感染不显著影响疟原虫的寄生虫密度在加纳的无症状感染输血

Hepatitis B Virus Infection Does Not Significantly Influence Plasmodium Parasite Density in Asymptomatic Infections in Ghanaian Transfusion Recipients 1 2 1 Graham Lee Freimanis , Shirley Owusu-Ofori , Jean-Pierre Allain * 1 Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, United Kingdom, 2 Transfusion Medicine Unit, Komfo Anokye Teaching Hospital, Kumasi, Ghana Abstract Background: Areas endemic for malaria and Hepatitis B virus (HBV) infection largely overlap geographically. A recent study has suggested the existence of an interaction between the two pathogens in symptomatic co-infected individuals on the South-American continent. We examined this issue in a hyperendemic area for both pathogens in sub-Saharan Africa. Methodology and Findings: Pre-transfusion samples from a retrospective cohort of 154 blood transfusion recipients were screened for both serological and molecular markers of HBV and Plasmodium genomes using species-specific nested PCR and quantitative real-time PCR. Thirty-seven individuals met exclusion criteria and were subsequently eliminated from further analysis. Of 117 participants, 90% of recipients exhibited evidence of exposure to HBV, 42% with HBsAg and/or HBV DNA and 48% anti-HBc reactive without detectable HBV DNA. Plasmodium genome prevalence by NAT was 50%. Parasitemic individuals were significantly younger than non-parasitemic individuals (P = 0.04). Parasitemia level was not significantly lower in individuals with HBV DNA positive infections compared to those with HBV DNA negative exposures. HBV DNA load was not significantly different in parasitemic and non-parasitemic individuals. Conclusion: The data presented suggests

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