Abstract

Hematopoietic stem cells (HSCs) are pivotal for maintaining blood cell production and immune function, and their dysregulation is implicated in hematological abnormalities observed in Human Immunodeficiency Virus (HIV) infection. GATA-1, a master transcription factor in hematopoietic development, plays a critical role in HSC maintenance, lineage commitment, and differentiation. This review explores the molecular mechanisms underlying the involvement of GATA-1 in HSC maintenance in the context of HIV infection and discusses its therapeutic implications. HIV infection is associated with disruptions in hematopoietic homeostasis, leading to bone marrow dysfunction and compromised immune function. GATA-1 dysregulation, influenced by chronic inflammation, viral replication, and antiretroviral therapy, contributes to aberrant hematopoietic signaling pathways. Understanding the role of GATA-1 in HSC maintenance offers potential therapeutic avenues for restoring hematopoietic function and ameliorating hematological abnormalities in HIV-infected individuals. Therapeutic strategies targeting GATA-1, including small molecule inhibitors and gene editing technologies, hold promise for mitigating the deleterious effects of GATA-1 dysregulation on HSCs. This review provides insights into the molecular mechanisms of GATA-1-mediated HSC maintenance in HIV infection and underscores the importance of further research to optimize therapeutic interventions and improve outcomes for affected individuals