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High-throughput Screening for Broad-spectrum Chemical Inhibitors of RNA Viruses

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A Phenotypic Screen Identifies Potent DPP9 Inhibitors Capable of Killing HIV-1 Infected Cells.

Keith P Moore¹, Adam G Schwaid¹, Matthew Tudor²

¹Chemical Biology, Merck & Co., Inc., Rahway, New Jersey 07065, United States.

ACS Chemical Biology

|August 31, 2022

Summary

Researchers discovered novel compounds that induce cell death in HIV-1 infected cells by targeting DPP9 and CARD8 inflammasome. This approach, synergistic with efavirenz, offers a potential strategy for HIV-1 eradication by engaging the pyroptotic pathway.

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Last Updated: Jun 19, 2026

High-throughput Screening for Broad-spectrum Chemical Inhibitors of RNA Viruses

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Published on: May 5, 2014

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

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Published on: December 21, 2019

Area of Science:

Virology
Immunology
Pharmacology

Background:

Current antiretroviral therapy (ART) effectively controls HIV-1 replication but does not eliminate persistent viral reservoirs, hindering curative strategies.
Eradicating latent HIV-1 reservoirs is a critical challenge for achieving a functional cure in people living with HIV-1 (PLWH).

Purpose of the Study:

To identify novel chemical compounds capable of eliminating HIV-1 infected cells.
To elucidate the mechanism of action of these compounds and their potential for synergistic therapy.

Main Methods:

Phenotypic screening to identify compounds targeting HIV-1 infected cells.
Chemoproteomic, biochemical, pharmacological, and genetic approaches to determine the mechanism of action.
In vitro synergy studies with efavirenz.

Main Results:

A novel chemical class, including compounds ICeD-1 and ICeD-2, was identified to kill HIV-1 infected peripheral blood mononuclear cells.
These compounds modulate dipeptidyl peptidase 9 (DPP9) and activate the caspase recruitment domain family member 8 (CARD8) inflammasome.
Efficacy was dependent on HIV-1 protease activity and synergistic with efavirenz, lowering its effective concentration.

Conclusions:

Engagement of the pyroptotic pathway via DPP9 modulation and CARD8 inflammasome activation presents a potential strategy for HIV-1 reservoir eradication.
The synergy between ICeD compounds and efavirenz suggests a promising therapeutic approach for achieving HIV-1 cure.