In vivo emergence of vicriviroc resistance in a human immunodeficiency virus type 1 subtype C-infected subject

J Virol. 2008 Aug;82(16):8210-4. doi: 10.1128/JVI.00444-08. Epub 2008 May 21.

Abstract

Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Anti-HIV Agents / pharmacology
  • Antibodies, Monoclonal / chemistry
  • CCR5 Receptor Antagonists
  • DNA Primers / chemistry
  • Drug Resistance, Viral*
  • HIV Infections / drug therapy*
  • HIV Infections / pathology
  • HIV-1 / metabolism*
  • Humans
  • Molecular Sequence Data
  • Piperazines / pharmacology*
  • Pyrimidines / pharmacology*
  • Receptors, CCR5 / metabolism
  • Recombination, Genetic
  • Sequence Homology, Amino Acid
  • Time Factors
  • Viral Envelope Proteins / chemistry

Substances

  • Anti-HIV Agents
  • Antibodies, Monoclonal
  • CCR5 Receptor Antagonists
  • DNA Primers
  • Piperazines
  • Pyrimidines
  • Receptors, CCR5
  • Viral Envelope Proteins
  • vicriviroc

Associated data

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