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A new class of multimerization selective inhibitors of HIV-1 integrase
Journal article   Open access   Peer reviewed

A new class of multimerization selective inhibitors of HIV-1 integrase

Amit Sharma, Alison Slaughter, Nivedita Jena, Lei Feng, Jacques J Kessl, Hind J Fadel, Nirav Malani, Frances Male, Li Wu, Eric Poeschla, …
PLoS pathogens, Vol.10(5), pp.e1004171-e1004171
05/2014
DOI: 10.1371/journal.ppat.1004171
PMCID: PMC4038613
PMID: 24874515
url
https://doi.org/10.1371/journal.ppat.1004171View
Published (Version of record) Open Access

Abstract

The quinoline-based allosteric HIV-1 integrase (IN) inhibitors (ALLINIs) are promising candidates for clinically useful antiviral agents. Studies using these compounds have highlighted the role of IN in both early and late stages of virus replication. However, dissecting the exact mechanism of action of the quinoline-based ALLINIs has been complicated by the multifunctional nature of these inhibitors because they both inhibit IN binding with its cofactor LEDGF/p75 and promote aberrant IN multimerization with similar potencies in vitro. Here we report design of small molecules that allowed us to probe the role of HIV-1 IN multimerization independently from IN-LEDGF/p75 interactions in infected cells. We altered the rigid quinoline moiety in ALLINIs and designed pyridine-based molecules with a rotatable single bond to allow these compounds to bridge between interacting IN subunits optimally and promote oligomerization. The most potent pyridine-based inhibitor, KF116, potently (EC50 of 0.024 µM) blocked HIV-1 replication by inducing aberrant IN multimerization in virus particles, whereas it was not effective when added to target cells. Furthermore, KF116 inhibited the HIV-1 IN variant with the A128T substitution, which confers resistance to the majority of quinoline-based ALLINIs. A genome-wide HIV-1 integration site analysis demonstrated that addition of KF116 to target or producer cells did not affect LEDGF/p75-dependent HIV-1 integration in host chromosomes, indicating that this compound is not detectably inhibiting IN-LEDGF/p75 binding. These findings delineate the significance of correctly ordered IN structure for HIV-1 particle morphogenesis and demonstrate feasibility of exploiting IN multimerization as a therapeutic target. Furthermore, pyridine-based compounds present a novel class of multimerization selective IN inhibitors as investigational probes for HIV-1 molecular biology.
HIV Integrase Inhibitors - pharmacology Cell Line Virus Replication - drug effects Antiviral Agents - pharmacology HIV-1 - drug effects Intercellular Signaling Peptides and Proteins - pharmacology Humans Protein Binding - drug effects Virus Integration - drug effects HIV Integrase - metabolism Protein Multimerization - drug effects Quinolines - pharmacology

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