REVIEW article
Front. Immunol.
Sec. Viral Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1621338
This article is part of the Research TopicHIV-1 Tat, An Enhancer of Virus Infectivity and Disease Promoter: Target for Preventive and Therapeutic InterventionsView all 6 articles
HIV-Tat and Vascular Endothelium: Implications in the HIV associated Brain, Heart, and Lung complications
Provisionally accepted- University of Kansas Medical Center, Kansas City, United States
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Following the advent of antiretroviral therapy (ART), neurological, cardiovascular, and pulmonary comorbidities emerged as major challenges in treating non-infectious complications in people living with HIV. Despite effective ART, HIV viral proteins can persist in circulation even in individuals with negligible viral loads, potentially contributing to cellular and tissue-level stress, inflammation, and related health complications. Most of the HIV protein: Tat (Trans activator of Transcription), expressed in HIV-infected cells, is actively secreted and exerts its pathological effects on non-infected cells, particularly impacting the vascular endothelium. This review focuses on the role and the underlying mechanisms of HIV-Tat in promoting endothelial dysfunction across the cardiovascular, pulmonary, and brain vasculature. Additionally, we discuss how HIV-Tat interacts synergistically with drugs of abuse to exacerbate endothelial damage. Importantly, the vascular damage caused by Tat is not fully mitigated by HAART, necessitating further mechanistic investigations and targeted therapeutic interventions. Additionally, cessation of drug abuse is indispensable for improving clinical outcomes and restoring vascular health in people living with HIV.
Keywords: Endothelium, Tat, blood brain barrier, Pulmonary vascular remodeling, Cardiovascular dysfunction
Received: 12 May 2025; Accepted: 21 Jul 2025.
Copyright: © 2025 Chandran, Chen, Kaur and Dhillon. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Navneet Kaur Dhillon, University of Kansas Medical Center, Kansas City, United States
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.