Abstract

GATA-1 mutations have been implicated in various hematological disorders, and emerging evidence suggests their association with HIV infection, leading to a spectrum of hematological abnormalities. This review explores the role of GATA-1 mutations in HIV-associated hematological disorders, elucidating their molecular mechanisms, clinical implications, and therapeutic considerations. GATA-1 mutations contribute to bone marrow failure syndromes, thrombocytopenia, and dyserythropoiesis in HIV-infected individuals, exacerbating cytopenias and compromising immune function. Understanding the molecular mechanisms underlying GATA-1 mutations in the context of HIV infection provides insights into disease pathogenesis and therapeutic strategies. Targeted therapies aimed at restoring GATA-1 function or mitigating its pathogenic effects may offer promise for improving outcomes in affected individuals. This review highlights the importance of elucidating the role of GATA-1 mutations in HIV-associated hematological disorders and underscores the need for further research to optimize therapeutic interventions.