Abstract

Hematopoietic stem cell (HSC) quiescence is crucial for maintaining the regenerative capacity of the hematopoietic system, and dysregulation of HSC quiescence has been implicated in hematological disorders, including those associated with Human Immunodeficiency Virus (HIV) infection. This review focuses on the role of GATA-1, a key transcription factor in hematopoiesis, in regulating HSC quiescence and its implications for therapy in HIV-infected individuals. We discuss the molecular mechanisms underlying GATA-1-mediated HSC quiescence, the impact of HIV on HSC function, and potential therapeutic strategies targeting GATA-1 to restore HSC homeostasis in HIV-infected individuals. Understanding the interplay between GATA-1 and HSC quiescence in the context of HIV infection may lead to the development of novel therapeutic approaches aimed at preserving hematopoietic function and improving clinical outcomes in HIV-infected individuals.