Abstract

Hemochromatosis, a disorder characterized by excessive iron absorption leading to systemic iron overload, and Human Immunodeficiency Virus (HIV), a viral infection targeting the immune system, represent significant health challenges worldwide. Concurrently, host genetic factors play a pivotal role in determining susceptibility to HIV infection and disease progression. Genetic polymorphisms affecting immune response pathways, viral entry receptors, and cytokine signaling pathways influence individual susceptibility and disease outcomes. Importantly, population-specific genetic variations contribute to differential HIV susceptibility and response to antiretroviral therapy, emphasizing the need for personalized approaches in HIV management. The intersection of hemochromatosis and HIV introduces unique challenges and clinical implications. Individuals with hemochromatosis may exhibit increased susceptibility to HIV infection due to dysregulated iron metabolism compromising immune function. Conversely, HIV infection can exacerbate iron dysregulation, leading to accelerated progression of hepatic and systemic complications in co-infected individuals. Understanding the intricate interplay between iron homeostasis, immune response, and viral pathogenesis is essential for optimizing therapeutic strategies and improving clinical outcomes in this vulnerable population. Unraveling the genetic susceptibility to hemochromatosis and HIV opens avenues for targeted interventions and preventive measures. Mechanistic insights into the complex interactions between iron metabolism and viral infection may inform the development of novel therapeutic approaches, including iron chelation therapy and immunomodulatory interventions, to mitigate the adverse effects of co-infection