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Anti‐ HIV ‐1 antibodies trigger non‐lytic complement deposition on infected cells
Author(s) -
Dufloo Jérémy,
GuivelBenhassine Florence,
Buchrieser Julian,
Lorin Valérie,
Grzelak Ludivine,
Dupouy Emilie,
Mestrallet Guillaume,
Bourdic Katia,
Lambotte Olivier,
Mouquet Hugo,
Bruel Timothée,
Schwartz Olivier
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201949351
Subject(s) - lytic cycle , antibody , complement (music) , virology , microbiology and biotechnology , biology , chemistry , virus , immunology , biochemistry , gene , phenotype , complementation
The effect of anti‐ HIV ‐1 antibodies on complement activation at the surface of infected cells remains partly understood. Here, we show that a subset of anti‐Envelope (Env) broadly neutralizing antibodies ( bNA bs), targeting the CD 4 binding site and the V3 loop, triggers C3 deposition and complement‐dependent cytotoxicity ( CDC ) on Raji cells engineered to express high surface levels of HIV ‐1 Env. Primary CD 4 T cells infected with laboratory‐adapted or primary HIV ‐1 strains and treated with bNA bs are susceptible to C3 deposition but not to rapid CDC . The cellular protein CD 59 and viral proteins Vpu and Nef protect infected cells from CDC mediated by bNA bs or by polyclonal IgGs from HIV ‐positive individuals. However, complement deposition accelerates the disappearance of infected cells within a few days of culture. Altogether, our results uncover the contribution of complement to the antiviral activity of anti‐ HIV ‐1 bNA bs.