AI Article Synopsis

  • HIV-1 uses the V3 loop of its envelope glycoprotein gp120 to recognize the CXCR4 coreceptor on host cells during viral entry.
  • Synthetic cyclic peptides mimicking the V3 loop were created to study their interactions with CXCR4, showing that both L- and D-amino acid versions bind selectively to CXCR4, but not to CCR5.
  • Molecular modeling revealed that specific negatively charged residues on CXCR4 facilitate favorable interactions with positively charged residues in the peptides, indicating a flexible binding mechanism that could help the virus adapt to mutations in the V3 loop.

Article Abstract

Human immunodeficiency virus-1 (HIV-1) recognizes one of its principal coreceptors, CXC chemokine receptor 4 (CXCR4), on the host cell via the third variable loop (V3 loop) of HIV-1 envelope glycoprotein gp120 during the viral entry process. Here, the mechanism of the molecular recognition of HIV-1 gp120 V3 loop by coreceptor CXCR4 was probed by synthetic peptides containing the full-length V3 loop. The two ends of the V3 loop were covalently linked by a disulfide bond to form a cyclic peptide with better conformational integrity. In addition, to probe the effect of the changed side-chain conformations of the peptide on CXCR4 recognition, an all-D-amino acid analog of the L-V3 loop peptide was generated. Both of these cyclic L- and D-V3 loop peptides displayed comparable binding recognition to the CXCR4 receptor, but not to another chemokine receptor, CCR5, suggesting their selective interactions with CXCR4. Molecular modeling studies revealed the important roles played by many negative-charged Asp and Glu residues on CXCR4 that probably engaged in favorable electrostatic interactions with the positive-charged Arg residues present in these peptides. These results support the notion that the HIV-1 gp120 V3 loop-CXCR4 interface is flexible for ligands of different chiralities, which might be relevant in terms of the ability of the virus to retain coreceptor recognition despite the mutations at the V3 loop.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10221217PMC
http://dx.doi.org/10.3390/v15051084DOI Listing

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