Hematopoietic stem cell (HSC) dysfunction is a significant contributor to immune impairment in HIV infection.
GATA-1, a pivotal transcription factor in hematopoiesis, emerges as a key regulator influencing HSC function and
lineage commitment. This review explores the intricate relationship between GATA-1 and HSCs in the context of
HIV, shedding light on potential therapeutic implications. We discuss the impact of GATA-1 dysregulation on
hematopoietic processes in HIV, highlighting its role in immune cell differentiation and activation. Furthermore, we
examine therapeutic strategies targeting GATA-1 to restore normal hematopoiesis and enhance immune reconstitution
in HIV-infected individuals. This comprehensive analysis underscores the importance of understanding GATA-1-
mediated mechanisms in shaping immune responses during HIV infection and emphasizes the therapeutic potential of
targeting GATA-1 for mitigating immune dysfunction and improving patient outcomes.