Beyond Viral Neutralization.

Journal Article (Journal Article;Review)

It has been known for more than 30 years that HIV-1 infection drives a very potent B cell response resulting in the production of anti-HIV-1 antibodies targeting several viral proteins, particularly its envelope glycoproteins (Env). Env epitopes are exposed on the surfaces of viral particles and infected cells where they are targets of potentially protective antibodies. These antibodies can interdict infection by neutralization and there is strong evidence suggesting that Fc-mediated effector function can also contribute to protection. Current evidence suggests that Fc-mediated effector function plays a role in protection against infection by broadly neutralizing antibodies and it might be important for protection by non-neutralizing antibodies. Fc-mediated effector function includes diverse mechanisms such as antibody-dependent cellular cytotoxicity (ADCC), antibody-mediated complement activation, antibody-dependent cellular phagocytosis, antibody-dependent cell-mediated virus inhibition, antibody-mediated trancytosis inhibition, and antibody-mediated virus opsonization. All these functions could be beneficial in fighting viral infections, including HIV-1. In this perspective, we discuss the latest developments in ADCC research discussed at the HIVR4P satellite session on non-neutralizing antibodies, with emphasis on the mechanisms of ADCC resistance used by HIV-1, the structural basis of epitopes recognized by antibodies that mediate ADCC, natural killer-cell education and ADCC, and murine models to study ADCC against HIV-1.

Full Text

Duke Authors

Cited Authors

  • Lewis, GK; Pazgier, M; Evans, DT; Ferrari, G; Bournazos, S; Parsons, MS; Bernard, NF; Finzi, A

Published Date

  • August 2017

Published In

Volume / Issue

  • 33 / 8

Start / End Page

  • 760 - 764

PubMed ID

  • 28084796

Pubmed Central ID

  • PMC5695748

Electronic International Standard Serial Number (EISSN)

  • 1931-8405

Digital Object Identifier (DOI)

  • 10.1089/AID.2016.0299


  • eng

Conference Location

  • United States