Next Article in Journal
Epstein–Barr Virus-Induced Post-Transplant Lymphoproliferative Disorder of the Central Nervous System Successfully Treated with Chemo-Immunotherapy
Next Article in Special Issue
Systems Biology Analysis of the Antagonizing Effects of HIV-1 Tat Expression in the Brain over Transcriptional Changes Caused by Methamphetamine Sensitization
Previous Article in Journal
Interaction between PHB2 and Enterovirus A71 VP1 Induces Autophagy and Affects EV-A71 Infection
Previous Article in Special Issue
Oxygen Levels Affect Macrophage HIV-1 Gene Expression and Delay Resolution of Inflammation in HIV-Tg Mice
Open AccessReview

Tat-Based Therapies as an Adjuvant for an HIV-1 Functional Cure

Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia
Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, QLD 4072, Australia
Author to whom correspondence should be addressed.
Viruses 2020, 12(4), 415;
Received: 28 February 2020 / Revised: 31 March 2020 / Accepted: 4 April 2020 / Published: 8 April 2020
(This article belongs to the Special Issue HIV-1 Transcription Regulation)
The human immunodeficiency virus type 1 (HIV) establishes a chronic infection that can be well controlled, but not cured, by combined antiretroviral therapy (cART). Interventions have been explored to accomplish a functional cure, meaning that a patient remains infected but HIV is undetectable in the blood, with the aim of allowing patients to live without cART. Tat, the viral transactivator of transcription protein, plays a critical role in controlling HIV transcription, latency, and viral rebound following the interruption of cART treatment. Therefore, a logical approach for controlling HIV would be to block Tat. Tackling Tat with inhibitors has been a difficult task, but some recent discoveries hold promise. Two anti-HIV proteins, Nullbasic (a mutant of Tat) and HT1 (a fusion of HEXIM1 and Tat functional domains) inhibit viral transcription by interfering with the interaction of Tat and cellular factors. Two small molecules, didehydro-cortistatin A (dCA) and triptolide, inhibit Tat by different mechanisms: dCA through direct binding and triptolide through enhanced proteasomal degradation. Finally, two Tat-based vaccines under development elicit Tat-neutralizing antibodies. These vaccines have increased the levels of CD4+ cells and reduced viral loads in HIV-infected people, suggesting that the new vaccines are therapeutic. This review summarizes recent developments of anti-Tat agents and how they could contribute to a functional cure for HIV. View Full-Text
Keywords: Tat; HIV transcription; Nullbasic; didehydro-cortistatin A; block and lock; HIV functional cure; Tat vaccine; triptolide Tat; HIV transcription; Nullbasic; didehydro-cortistatin A; block and lock; HIV functional cure; Tat vaccine; triptolide
Show Figures

Graphical abstract

MDPI and ACS Style

Jin, H.; Li, D.; Lin, M.-H.; Li, L.; Harrich, D. Tat-Based Therapies as an Adjuvant for an HIV-1 Functional Cure. Viruses 2020, 12, 415.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Search more from Scilit
Back to TopTop