Publications

Hemochromatosis and HIV infection represent distinct yet intersecting conditions with significant implications for immune senescence, the gradual decline in immune function associated with aging. Hemochromatosis, characterized by excessive iron accumulation in tissues, and HIV infection, a chronic viral illness leading to progressive immune dysfunction, both contribute to immune dysregulation and accelerated aging of the immune system. This review explores the complex interplay between hemochromatosis, HIV infection, and immune senescence, highlighting the underlying mechanisms, clinical implications, and potential therapeutic strategies. Excess iron accumulation in hemochromatosis promotes oxidative stress, inflammation, and tissue damage, accelerating cellular aging and immune dysfunction. Iron overload affects immune cell function at multiple levels, including impairment of T cell and B cell responses, dysregulation of macrophage activity, and disruption of immune signaling pathways. Moreover, iron-mediated inflammation exacerbates immune senescence by promoting chronic activation of the innate and adaptive immune systems, contributing to the pathogenesis of age-related diseases and increasing susceptibility to infections in hemochromatosis patients. In HIV infection, chronic viral replication, and immune activation drive immune exhaustion, depletion of CD4+ T cells, and dysfunction of the immune system, leading to accelerated immune senescence. HIV-associated inflammation and viral persistence further exacerbate immune dysfunction and contribute to the premature aging of the immune system. The intersection of hemochromatosis and HIV infection exacerbates immune senescence, as iron overload and chronic inflammation synergis