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Anti-phospholipid human monoclonal antibodies inhibit CCR5-tropic HIV-1 and induce beta-chemokines.

  • Author(s): 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
  • et al.
Abstract

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.

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