Abstract

Myelodysplastic syndromes (MDS) pose a significant clinical challenge in individuals with Human Immunodeficiency Virus (HIV) infection, characterized by dysregulated hematopoiesis and an increased risk of progression to acute myeloid leukemia (AML). Emerging evidence suggests an association between MDS and HIV infection, prompting a deeper exploration of the underlying pathogenic mechanisms and treatment strategies for this hematological complication. This review examines the role of GATA-1, a master transcription factor in hematopoiesis, in the pathogenesis of HIV-associated MDS and discusses current treatment approaches. Dysregulated GATA-1 activity may contribute to the development and progression of MDS in HIV-infected individuals by promoting aberrant hematopoietic differentiation and impairing stem cell function. Understanding the molecular mechanisms underlying GATA-1 dysregulation in HIV-associated MDS is crucial for elucidating disease pathogenesis and identifying potential therapeutic targets. Treatment strategies for HIV-associated MDS may include supportive care measures, such as blood transfusions and growth factor support, as well as disease-modifying therapies, such as hypomethylating agents and immunosuppressive therapy. Further research is needed to optimize treatment approaches for this complex hematological complication and improve outcomes for affected individuals.