Highly potent RANTES analogues either prevent CCR5-using human immunodeficiency virus type 1 infection in vivo or rapidly select for CXCR4-using variants

J Virol. 1999 May;73(5):3544-50. doi: 10.1128/JVI.73.5.3544-3550.1999.

Abstract

The natural ligands for the CCR5 chemokine receptor, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and RANTES (regulated on T-cell activation, normal T-cell expressed and secreted), are known to inhibit human immunodeficiency virus (HIV) entry, and N-terminally modified RANTES analogues are more potent than native RANTES in blocking infection. However, potent CCR5 blocking agents may select for HIV-1 variants that use alternative coreceptors at less than fully inhibitory concentrations. In this study, two N-terminal chemical modifications of RANTES produced by total synthesis, aminooxypentane (AOP)-RANTES[2-68] and N-nonanoyl (NNY)-RANTES[2-68], were tested for their ability to prevent HIV-1 infection and to select for coreceptor switch variants in the human peripheral blood lymphocyte-SCID mouse model. Mice were infected with a CCR5-using HIV-1 isolate that requires only one or two amino acid substitutions to use CXCR4 as a coreceptor. Even though it achieved lower circulating concentrations than AOP-RANTES (75 to 96 pM as opposed to 460 pM under our experimental conditions), NNY-RANTES was more effective in preventing HIV-1 infection. However, in a subset of treated mice, these levels of NNY-RANTES rapidly selected viruses with mutations in the V3 loop of envelope that altered coreceptor usage. These results reinforce the case for using agents that block all significant HIV-1 coreceptors for effective therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Anti-HIV Agents / chemical synthesis
  • Anti-HIV Agents / pharmacology*
  • Chemokine CCL5 / analogs & derivatives*
  • Chemokine CCL5 / chemical synthesis
  • Chemokine CCL5 / pharmacology
  • Disease Models, Animal
  • Genetic Variation
  • HIV Infections / immunology
  • HIV Infections / metabolism
  • HIV Infections / virology*
  • HIV-1 / drug effects*
  • HIV-1 / genetics
  • HIV-1 / metabolism
  • Humans
  • Mice
  • Mice, SCID
  • Molecular Sequence Data
  • Receptors, CCR5 / metabolism*
  • Receptors, CXCR4 / metabolism*
  • Sequence Homology, Amino Acid

Substances

  • Anti-HIV Agents
  • Chemokine CCL5
  • Receptors, CCR5
  • Receptors, CXCR4
  • aminooxypentane-RANTES