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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

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Synergistic Chromatin-Modifying Treatments Reactivate Latent HIV and Decrease Migration of Multiple Host-Cell Types.

Alexandra Blanco¹, Tarun Mahajan¹, Robert A Coronado¹

¹Department of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.

|July 2, 2021

Summary

Latency reversal agents (LRAs) can reactivate latent human immunodeficiency virus (HIV) in monocytes. These treatments affect HIV reactivation and cell migration, crucial for "Shock and Kill" therapy.

Keywords:

LTR promoter T cells chromatin modifier human immunodeficiency virus latency reversal monocytes

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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

Area of Science:

Virology
Immunology
Cell Biology

Background:

Human immunodeficiency virus (HIV) establishes a latent reservoir in various cell types, hindering curative strategies.
Latency reversal agents (LRAs) aim to reactivate HIV from this dormant state for elimination.

Purpose of the Study:

To investigate the efficacy of LRAs in reversing HIV latency in THP-1 monocytes.
To analyze the impact of LRAs on HIV long terminal repeat (LTR) promoter activation and cell migration.

Main Methods:

Established an in vitro HIV latency model using THP-1 monocytes and a replication-incompetent HIV reporter vector.
Assessed the synergistic effects of chromatin modifiers and transcriptional activators on HIV reactivation.
Measured surface expression of chemokine receptor type 4 (CXCR4) and its effect on cell migration.

Main Results:

Leading LRA treatments synergistically activated the HIV LTR promoter in monocytes.
Chromatin modifiers combined with transcriptional activators enhanced HIV reactivation, mirroring T-cell responses.
Reactivation cocktails differentially impacted latency reversal and CXCR4 expression, altering monocyte migration.

Conclusions:

Epigenetic mechanisms in monocytes play a role in regulating HIV latency reversal and cell migration.
Understanding these mechanisms is vital for developing effective "Shock and Kill" therapies targeting diverse HIV reservoirs.