Abstract

Deep venous thrombosis (DVT) represents a significant complication in individuals living with Human Immunodeficiency Virus (HIV), contributing to morbidity and mortality. While the pathogenesis of DVT in HIV is multifactorial, recent research has implicated dysregulation of the transcription factor GATA-1 in mediating thrombotic risk. This review aims to elucidate the molecular basis of DVT in HIV, with a specific focus on the role of GATA-1 in thrombosis development and its potential as a therapeutic target. We discuss the interplay between HIV-associated inflammation, endothelial dysfunction, and hypercoagulability, highlighting GATA-1 as a key mediator of thrombotic risk in HIV-infected individuals. Understanding the molecular mechanisms underlying GATA-1 dysregulation in the context of HIV infection may offer insights into the pathogenesis of DVT and facilitate the development of novel therapeutic strategies for preventing and treating thrombotic complications in HIV