- Moody, M Anthony;
- Liao, Hua-Xin;
- Alam, S Munir;
- Scearce, Richard M;
- Plonk, M Kelly;
- Kozink, Daniel M;
- Drinker, Mark S;
- Zhang, Ruijun;
- Xia, Shi-Mao;
- Sutherland, Laura L;
- Tomaras, Georgia D;
- Giles, Ian P;
- Kappes, John C;
- Ochsenbauer-Jambor, Christina;
- Edmonds, Tara G;
- Soares, Melina;
- Barbero, Gustavo;
- Forthal, Donald N;
- Landucci, Gary;
- Chang, Connie;
- King, Steven W;
- Kavlie, Anita;
- Denny, Thomas N;
- Hwang, Kwan-Ki;
- Chen, Pojen P;
- Thorpe, Philip E;
- Montefiori, David C;
- Haynes, Barton F
Traditional 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.