Disruption of blood-brain barrier: effects of HIV Tat on brain microvascular endothelial cells and tight junction proteins

Although the widespread use of antiretroviral therapy (ART) has prolonged the life span of people living with HIV (PLWH), the incidence of HIV-associated neurocognitive disorders (HAND) in PLWH is also gradually increasing, seriously affecting the quality of life for PLWH. However, the pathogenesis of HAND has not been elucidated, which leaves HAND without effective treatment. HIV protein transactivator of transcription (Tat), as an important regulatory protein, is crucial in the pathogenesis of HAND, and its mechanism of HAND has received widespread attention. The blood-brain barrier (BBB) and its cellular component brain microvascular endothelial cells (BMVECs) play a necessary role in protecting the central nervous system (CNS), and their damage associated with Tat is a potential therapeutic target of HAND. In this review, we will study the Tat-mediated damage mechanism of the BBB and present multiple lines of evidence related to BMVEC damage caused by Tat.

Automated summary

Despite the prolongation of lifespan in people living with HIV (PLWH) due to antiretroviral therapy (ART), the incidence of HIV-associated neurocognitive disorders (HAND) is gradually increasing, greatly impacting the quality of life for PLWH. The pathogenesis of HAND, specifically its mechanism involving the HIV protein transactivator of transcription (Tat), remains unclear. This review focuses on the Tat-mediated damage mechanism of the blood-brain barrier (BBB) and its cellular component, brain microvascular endothelial cells (BMVECs), and presents various evidence related to Tat-induced BMVEC damage.