Commentary 10.1172/JCI132535
1Emory Vaccine Center,
2Yerkes National Primate Center, and
3Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, USA.
Address correspondence to: Cynthia A. Derdeyn, Emory University, Yerkes National Primate Research Center, 954 Gatewood Rd., Atlanta, Georgia 30329, USA. Phone: 404.727.8594; Email: cderdey@emory.edu.
Find articles by Charles, T. in: JCI | PubMed | Google Scholar
1Emory Vaccine Center,
2Yerkes National Primate Center, and
3Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, USA.
Address correspondence to: Cynthia A. Derdeyn, Emory University, Yerkes National Primate Research Center, 954 Gatewood Rd., Atlanta, Georgia 30329, USA. Phone: 404.727.8594; Email: cderdey@emory.edu.
Find articles by Derdeyn, C. in: JCI | PubMed | Google Scholar
First published October 7, 2019 - More info
With almost 2 million new HIV-1 infections in 2018, a highly effective vaccine is imperative. Vaccine-elicited HIV-1 antibodies contribute to protection through multiple nonneutralizing activities, but the exact mechanisms remain unknown. In this issue of the JCI, Neidich and associates sought to determine how antibodies contributed to reducing the risk of HIV-1 acquisition in a phase IIb preventative vaccine efficacy trial, HVTN 505. Their studies revealed that antibody-dependent cellular phagocytosis (ADCP) and FcγRIIa binding were strongly associated with reduced HIV-1 risk; however, HIV-1 envelope–specific IgG3, IgA; and host FcγRIIa genotype also influenced risk. This study highlights the intricate interactions between antibodies and innate immune functions in humans.
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