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Sickle cell anaemia is single point mutation in position 6 of globin chain by valine replacing glutamic acid resulting to sickling and polymerization of red blood cells. This affects the supply of oxygen and vaso-occulisve crisis may set causing many systemic damages and creates great burden to the parents and the entire society.The burden of sickle cell anaemia is still high in Africa not minding the level of awareness in the society. The selective protective advantage of protection of sickle cell trait due the endemicity of malaria may be a major factor on the burden level in Africa as well as some culture. More sickle cell education should be given in public places and included in the curriculum of different levels of education for prevention.

Co-infection with HIV and malaria presents a multifaceted clinical scenario with intricate immunological interplays, wherein neutrophils, the primary mediators of innate immunity, emerge as pivotal actors. This paper aims to comprehensively analyze the dynamic role of neutrophils in the progression of HIV within the context of malaria co-infection. Neutrophils, conventionally viewed as short-lived effectors, exhibit remarkable plasticity and multifunctionality, contributing significantly to immune responses during co-infections. Their phenotype and functions undergo profound alterations in response to the complex milieu of both HIV and malaria, impacting disease progression and immunomodulation. This paper scrutinizes the nuanced alterations in neutrophil phenotypes, their diverse effector functions, and their contributions to immunopathogenesis within the HIV-malaria co-infection paradigm. Neutrophils, driven by dysregulated cytokines and inflammatory cues, exhibit heightened activation, potentially exacerbating tissue damage and chronic immune activation. Insights gleaned from understanding neutrophil dynamics in this co-infection scenario hold significant therapeutic implications. Potential interventions targeting neutrophil responses offer promising avenues for modulating immune dysregulation and managing disease progression. The review underscores the need for innovative therapeutic approaches aimed at harnessing neutrophil functionalities to mitigate HIV progression within malaria co-infected individuals. In conclusion, unraveling the intricate roles of neutrophils provides critical insights into the immunopathogenesis of HIV within the context of malaria co-infection. This comprehensive understanding not only sheds light on immune modulation but also presents a foundation for future therapeutic strategies aimed at improving clinical outcomes in this complex co-infection scenario.

Platelets, conventionally recognized for their pivotal roles in hemostasis and thrombosis, have emerged as multifunctional players in immune responses. In the context of Human Immunodeficiency Virus (HIV) infection, platelets exhibit intricate interactions influencing viral pathogenesis, immune activation, and disease progression. This review aims to provide an in-depth analysis of the diverse roles played by platelets in modulating HIV infection, shedding light on their impact on viral dynamics, immune responses, and associated pathophysiological processes. The paper addresses platelet-driven alterations in coagulation pathways and endothelial function in the context of HIV, emphasizing their role in HIV-associated coagulopathies, endothelial activation, and consequent vascular dysfunction. Additionally, the involvement of platelets in the development of HIV-associated comorbidities such as cardiovascular complications, neurocognitive impairment, and systemic inflammation is discussed, delineating platelet-driven mechanisms contributing to the pathogenesis of these conditions and their implications for disease outcomes. In conclusion, the multifaceted roles of platelets in HIV infection underscore their significance beyond hemostasis, offering potential insights into therapeutic avenues and highlighting the need for further investigations to decode the complexity of platelet-driven modulation of HIV infection.