A Highly-Conserved Residue of the HIV-1-gp120 Inner Domain is Important for ADCC Responses Mediated by Anti-Cluster A Antibodies

Creators: Ding, Shilei; Veillete, Maxime; Coutu, Mathieu; Prévost, Jéremie; Scharf, Louise; Bjorkman, Pamela J.; Ferrari, Guido; Robinson, James E.; Stürzel, Christina; Hahn, Beatrice H.; Sauter, Daniel; Kirchhoff, Frank; Lewis, George K.; Pazgier, Marzena; Finzi, Andrés

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Abstract

Previous studies have shown that sera from HIV-1-infected individuals contain antibodies able to mediate antibody-dependent cellular cytotoxicity (ADCC). These antibodies preferentially recognize envelope glycoprotein (Env) epitopes induced upon CD4 binding. Here, we show that a highly conserved tryptophan at position 69 of the gp120 inner domain is important for ADCC mediated by anti-cluster A antibodies and sera from HIV-1-infected individuals.

Additional Information

© 2015 American Society for Microbiology. Received 30 October 2015; Accepted 30 November 2015; Accepted manuscript posted online 4 December 2015. We thank the CRCHUM Flow Cytometry Platform for technical assistance as well as Mario Legault for cohort coordination. We are thankful for subjects' participation and collaboration. We thank Yongjun Guan for providing the gp41 antibodies and their clones. We thank Jonathan Richard for helpful discussions. We thank Pascal Poignard and IAVI for kindly providing PGT151, Gunilla Karlsson Hedestam and Ganesh Phad for GE2-JG8, and the NIH AIDS Reagent Program, Division of AIDS, NIAID, NIH, for CD4-binding site VRC01 (John Mascola) and b12 (Dennis Burton and Carlos Barbas) MAbs. We also thank David Evans for the CEM.NKr cell line. This work was supported by a Canada Foundation for Innovation Program Leader grant, by CIHR operating grants 119334 and 134117, by an FRQS Establishment of Young Scientist grant 26702 to A.F., by the FRQS AIDS and Infectious Diseases Network, and by NIH AI100645 Center for HIV/AIDS Vaccine Immunology and Immunogen Design (CHAVI-ID). A.F. is the recipient of a Canada Research Chair on Retroviral Entry. M.V. was supported by CIHR Doctoral Research award 291485. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have no conflicts of interest to report.

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