Moody, MALiao, HXAlam, SMScearce, RMPlonk, MKKozink, DMDrinker, MSZhang, RXia, SMSutherland, LLTomaras, GDGiles, IPKappes, JCOchsenbauer Jambor, CEdmonds, TGSoares, MBarbero, GForthal, DNLanducci, GChang, CKing, SWKavlie, ADenny, TNHwang, KKChen, PPThorpe, PEMontefiori, DCHaynes, BF2017-06-022017-06-022010-04-12https://hdl.handle.net/10161/14734Traditional antibody-mediated neutralization of HIV-1 infection is thought to result from the binding of antibodies to virions, thus preventing virus entry. However, antibodies that broadly neutralize HIV-1 are rare and are not induced by current vaccines. We report that four human anti-phospholipid monoclonal antibodies (mAbs) (PGN632, P1, IS4, and CL1) inhibit HIV-1 CCR5-tropic (R5) primary isolate infection of peripheral blood mononuclear cells (PBMCs) with 80% inhibitory concentrations of <0.02 to approximately 10 microg/ml. Anti-phospholipid mAbs inhibited PBMC HIV-1 infection in vitro by mechanisms involving binding to monocytes and triggering the release of MIP-1alpha and MIP-1beta. The release of these beta-chemokines explains both the specificity for R5 HIV-1 and the activity of these mAbs in PBMC cultures containing both primary lymphocytes and monocytes.Antibodies, AntiphospholipidAntibodies, MonoclonalCD4-Positive T-LymphocytesCardiolipinsCell FusionChemokine CCL3Chemokine CCL4ChemokinesChemokines, CCComplementarity Determining RegionsCulture Media, ConditionedEndotoxinsEpithelial CellsGiant CellsHIV-1HumansImmunity, InnateImmunoglobulin Fab FragmentsImmunoglobulin Fc FragmentsKineticsLeukocytes, MononuclearMonocytesMutationPhosphatidylethanolaminesPhosphatidylserinesReceptors, CCR5Viral TropismVirus Internalizationbeta 2-Glycoprotein Ienv Gene Products, Human Immunodeficiency VirusJournal article1540-9538