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HIV-1 integrase multimerization as a therapeutic target.

Lei Feng1, Ross C Larue, Alison Slaughter

  • 1The Center for Retrovirus Research and College of Pharmacy, The Ohio State University, Columbus, OH, 43210, USA.

Current Topics in Microbiology and Immunology
|March 18, 2015
PubMed
Summary
This summary is machine-generated.

Allosteric integrase inhibitors (ALLINIs) disrupt human immunodeficiency virus type 1 (HIV-1) assembly by causing aberrant multimerization of the integrase (IN) protein. This leads to non-infectious virus particles, highlighting IN multimerization as a therapeutic target.

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Area of Science:

  • Virology
  • Structural Biology
  • Drug Discovery

Background:

  • Multimeric human immunodeficiency virus type 1 (HIV-1) integrase (IN) is crucial for viral replication and a key therapeutic target.
  • Ordered interplay between IN subunits is essential for its function, including forming stable synaptic complexes (SSCs) for DNA integration.
  • LEDGF/p75, a cellular protein, binds the IN tetramer in the SSC and directs viral integration into active genes.

Purpose of the Study:

  • To investigate the mechanism of allosteric IN inhibitors (ALLINIs) in deregulating IN subunit interplay.
  • To explore the impact of ALLINIs on HIV-1 replication, focusing on integration and virus particle maturation.
  • To evaluate IN multimerization as a therapeutic target for novel HIV-1 inhibitors.

Main Methods:

  • Biochemical and structural studies of HIV-1 integrase (IN) and its interactions.
  • In vitro assays to assess SSC formation, LEDGF/p75 binding, and IN catalytic activities.
  • Analysis of virus particle maturation and infectivity in ALLINI-treated infected cells.

Main Results:

  • ALLINIs bind to the IN dimer interface, stabilizing IN subunits and promoting aberrant higher-order IN multimerization.
  • ALLINIs impair SSC formation, LEDGF/p75-independent IN activities, and LEDGF/p75 binding to the SSC in vitro.
  • In infected cells, ALLINIs more potently inhibited virus particle maturation than integration, inducing aberrant IN multimerization in virions and resulting in non-infectious particles.

Conclusions:

  • Aberrant IN multimerization induced by ALLINIs disrupts HIV-1 particle morphogenesis.
  • Targeting IN multimerization is a promising strategy for developing new HIV-1 inhibitors.
  • ALLINIs offer a novel therapeutic approach by interfering with essential IN functions beyond integration.