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Related Experiment Video

Updated: Jun 10, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

Resistance to integrase inhibitors.

Mathieu Métifiot¹, Christophe Marchand, Kasthuraiah Maddali

¹Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892, USA.

|August 14, 2010

Summary

Mutations in human immunodeficiency virus integrase (IN) cause treatment failure. Understanding IN resistance mutations, particularly in the flexible loop, is key to developing new antiviral drugs.

Keywords:

AIDS Elvitegravir GSK-1265744 GSK-1349572 HIV-1 integrase Raltegravir interfacial inhibitors resistance

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Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

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Published on: February 22, 2017

Area of Science:

Virology
Drug Discovery
Structural Biology

Background:

Integrase (IN) is a validated target for treating human immunodeficiency virus (HIV) infections.
Raltegravir and elvitegravir are advanced IN inhibitors, but treatment failure occurs due to resistant viral strains.
Mutations in the IN coding sequence can lead to cross-resistance, necessitating further characterization.

Purpose of the Study:

To review the structural and biochemical basis of IN resistance.
To highlight the role of the IN flexible loop (residues G140-G149) in drug action and resistance.
To inform the development of next-generation IN inhibitors to overcome drug resistance.

Main Methods:

Review of existing structural and biochemical data on HIV integrase.
Analysis of mutation patterns conferring drug resistance.
Focus on the functional significance of the IN flexible loop.

Main Results:

Specific mutations within the IN coding sequence confer cross-resistance to existing inhibitors.
The flexible loop region of IN (G140-G149) plays a crucial role in inhibitor binding and resistance development.
Structural and biochemical insights reveal mechanisms of resistance.

Conclusions:

Characterizing IN resistance mutations is critical for advancing HIV therapy.
Targeting the IN flexible loop may offer strategies for overcoming resistance.
Further development of second-generation IN inhibitors is needed to combat resistant HIV strains.