Background: Malaria and human immunodeficiency virus (HIV) are two major infections with enormous public health consequence. Together, they are endemic in many developing countries with anaemia being the most frequent haematological consequence of the infections. Objective: To determine the prevalence of malaria and HIV co-infection as well as anaemia among selected patients from three health-care institutions in Lagos, Nigeria. Methods: A cross-sectional study of 1080 patients was carried out to determine the prevalence of malaria and HIV coinfection as well as anaemia. Blood sera from each of the patients were screened for malaria parasites, HIV-1 and HIV-2 using Giemsa stain, Cambridge Biotech Recombigen HIV-1/HIV-2 rapid device, respectively while haemoglobin estimation was performed using cyanmethemoglobin method. Results: Our data showed that the total number of malaria infected patients were significantly higher in HIV sero-positive patients 47.7% (31/65) when compared with their HIV sero-negative counterparts 25.8% (262/1015) P = 0.047. The result also revealed that 25.8% (8/31) of the patients co-infected with malaria and HIV had anaemia as compared to 11.1% (29/ 262) infected with malaria alone. Multivariable logistic regression analysis showed that patients with dual infection of malaria and HIV were twice likely to be anaemic than those infected with malaria alone [adjusted OR 2.4, 95% CI, 1.3 to 2.7, P = 0.014]. Conclusion: Our data indicated a higher prevalence of malaria in HIV infected patients and also revealed that patients coinfected with malaria and HIV were more likely to be anaemic.

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Human infection by either Trypanosoma brucei gambiense (Tbg) or Trypanosoma brucei rhodesiense (Tbr) and the establishment of disease is made possible by the intermittent switching of their variant surface glycoprotein (VSG) and expression of serum resistance associated (SRA) protein (by Tbr) which nullifies the lytic action of the normal human serum. The ability to switch expression from one VSG to the other is recognized to be the major mechanism that permits the parasite to evade the otherwise efficient host antibody, hence preventing parasite elimination and allowing the establishment of a chronic infection. These changes were reported to: disable the host's capacity to mount a protective anti-parasite antibody response and prevent the development of effective B-cell memory against encountered variant antigenic parasite types (VATs). Both B cell-mediated antibody response and the Th1 cell responses leading to the production of interferon-gamma (IFN-) are required for maximum host resistance to trypanosomes, with IFN-acting to induce macrophage trypanolytic and trypanostatic activities. High levels of both tumor necrosis factor alpha (TNF) and interleukin 10 (IL-10) have been associated with trypanosomal infection. Trypanosomal genetics (including the parasite's intrinsic characteristics), human immune response polymorphisms and geographical locations are important elements that describe the severity or mildness of HAT. As the parasite devices ways to evade the human immune system, and in the absence of a suitable vaccine, surveillance, prompt diagnosis and treatment with available drugs and vector control efforts will go along way in reducing the incidence of HAT.

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