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American Society for Microbiology, Antimicrobial Agents and Chemotherapy, 2(54), p. 734-741, 2010

DOI: 10.1128/aac.00841-09

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Epitope Switching as a Novel Escape Mechanism of HIV to CCR5 Monoclonal Antibodies

Journal article published in 2010 by Andreas Jekle, Milloni Chhabra, Adriane Lochner, Sonja Meier ORCID, Eugene Chow, Michael Brandt, Surya Sankuratri, Nick Cammack, Gabrielle Heilek
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

ABSTRACT In passaging experiments, we isolated HIV strains resistant to MAb3952, a chemokine (C-C motif) receptor 5 (CCR5) monoclonal antibody (MAb) that binds to the second extracellular domain (extracellular loop 2 [ECL-2]) of CCR5. MAb3952-resistant viruses remain CCR5-tropic and are cross-resistant to a second ECL-2-specific antibody. Surprisingly, MAb3952-resistant viruses were more susceptible to RoAb13, a CCR5 antibody binding to the N terminus of CCR5. Using CCR5 receptor mutants, we show that MAb3952-resistant virus strains preferentially use the N terminus of CCR5, while the wild-type viruses preferentially use ECL-2. We propose this switch in the CCR5 binding site as a novel mechanism of HIV resistance.