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Author(s): Outoor H Taha¹1, Amna B Hamadnaallah²2, Danya H Taha23, Hind H Taha34, Wahaj M. Mohammed45, Abdelhakam H Ali56, Salah Marajan57, Abdulbasit Faraj Hadhr68

Email(s): 1daniataha78@gmail.com

Address:

    1. The National University, Khartoum, Sudan, Faculty of Medical Laboratory Science, Department of Parasitology. 2. The National University, Khartoum, Sudan, Faculty of Medical Laboratory Science, Department of Microbiology. 2. Sudan University of Science and Technology, Khartoum, Sudan, Faculty of Pharmacy, Department of Pharmacognosy. 3. University of Kordofan, Al-Ubayyid, Sudan, Faculty of Medicine, Department of Obstetrics and Gynecology. 4. Shendi University, Shendi, Sudan, Faculty of Medical Laboratory Science, Department of Parasitology. 5. University of Al Butana, Gezira, Sudan, Faculty of Medical Laboratory Science, Department of Microbiology. 5. The National University, Khartoum, Sudan, Faculty of Medical Laboratory Science, Department of Microbiology. 6. Oassar International University, Libya, Saraj Ealem Institute of Medical Science, Libya.

Published In:   Volume - 5,      Issue - 3,     Year - 2026

DOI: https://doi.org/10.71431/IJRPAS.2026.5308  

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ABSTRACT:
Background: Malaria and hepatitis b co infections are increasingly recognized developing countries. In many endemic setting, the overlap of chronic hepatitis virus (HBV) and P. falciparum infections is common, and an increased prevalence, from 0.7% to 1.7%, of this co-infection has been reported in Sudan. Immunologically, both pathogen may also overlap, as each is observed to mainly trigger T helper type 1 (Th1) cytokine responses. This study therefore estimate the cytokine profiles in Malaria and HBV co-infected individuals. Objectives This study therefore estimate the cytokine profiles in Malaria and HBV co-infected individuals Methods: Cytokine profiles were assayed and compared across four categories of chronic hepatitis b infected and malaria co-infected individuals : un-infected, mono-infected with Plasmodium falciparum (Malaria group), mono-infected with chronic hepatitis B virus (CHB group) and co-infected (Malaria +CHB group) using ELISA techniques. Results: The Malaria+CHB group had significantly concentration, [P<0.05 for all comparisons. In individual elevated with IL-10 falciparum Malaria+CHB, correlation analysis showed significant negative association of the pro-inflammatory IL-10 responses with malaria parasitemia. (P = 0.002; r = 0.479). Also, for individual with mixed infection in the Malaria+CHB group, parasitemia was observed to diminish HBV viremia [P = 0.003, r = -0.489]. Conclusion: Taken together the findings suggests that Malaria+CHB could aggravate inflammatory cytokine responses and increase susceptibility to liver injury among infected individuals in endemic settings.

Cite this article:
Outoor H Taha et al. Analysis of pro inflammatory cytokinse response among hepatitis B patients co-infected with Plasmodium falciparum in Khartoum state, Sudan. IJRPAS, March 2026; 5(3): 113-124.DOI: https://doi.org/https://doi.org/10.71431/IJRPAS.2026.5308


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