- Emmanuel Ifeanyi Obeagu* and Priya Homa Chukwu**
- 1Department of Biomedical and Laboratory Science, Africa University, Zimbabwe, 2Department of Haematology and Blood Transfusion Science, Faculty of Medical Laboratory Science, Rivers State University of Science and Technology, Port Harcourt, Rivers State.
- FAR Journal of Advanced Medical Studies (FARJAMS)
Abstract
HIV-positive individuals with sickle cell anemia (SCA) face unique immunological challenges due to the combined effects of viral-induced immune suppression and chronic inflammation associated with SCA. HIV depletes CD4+ T cells, impairing adaptive immunity, while SCA promotes persistent immune activation through hemolysis, endothelial dysfunction, and cytokine overproduction. Together, these conditions exacerbate immune dysregulation, increasing susceptibility to infections, immune exhaustion, and inflammatory complications. The coinfection of HIV and SCA alters innate and adaptive immune responses, leading to defective neutrophil and monocyte function, suboptimal vaccine responses, and an increased risk of opportunistic infections. Functional asplenia in SCA further compromises the ability to clear encapsulated bacteria, making bacterial infections a significant concern. Additionally, HIV-induced dysregulation of B and T cell function impairs antibody responses, further reducing immune protection. These compounded effects create significant clinical and therapeutic challenges in managing infections and inflammation in affected individuals.
