Research done by Tony Moody of Duke University under a CHAVI grant was presented at the 2008 Cape Town aids conference. In his oral abstract 0A03-06 found on page 57 at this link, the mab was referred to as PGN632.
"OA03-06 Anti-lipid Human Monoclonal Antibodies Inhibit HIV-1 Infection of PBMC by Binding to Host Cells MA Moody1, MK Plonk1, L Fuller1, H Liao1, S Xia1, MS Drinker1, TC Gurley1, RM Scearce1, GD Tomaras1, C Chang2, S King2, A Kavlie3, PE Thorpe4, SM Alam1, PP Chen5, DC Montefiori6, and BF Haynes1 1Duke University Medical Center, Durham, NC, USA; 2Peregrine Pharmaceuticals, Tustin, CA, USA; 3Affitech AS, Oslo, N-0349, Norway; 4University of Texas Southwestern Medical Center, Dallas, TX, USA; 5UCLA School of Medicine, Los Angeles, CA, USA; 6Department of Surgery, Duke University Medical Center, Durham, NC, USA Background: HIV-1-infected or vaccinated humans rarely make broadly-reactive neutralizing antibodies. Some antibodies against conserved Env epitopes share similarities with autoantibodies; one hypothesis is such antibodies are downregulated by immune tolerance. The observation that AIDS may be rare in primary autoimmune disease patients (1) prompted the hypothesis that autoimmune disease patients with defective tolerance mechanisms may make antibodies that in some manner protect against HIV-1 infection. Methods: We studied a panel of human anti-lipid mAbs from autoimmune disease patients and healthy controls. Mabs IS4, CL1, P1, and PGN632 bind cardiolipin and phosphatidylserine independent of β2-glycoprotein I; mAbs B1, B2, PGN634, and PGN635 require β2-glycoprotein I for lipid binding. Inhibition of HIV-1 infection was studied using HIV-1 Env pseudoviruses in TZM/bl cells and using whole virus assays in peripheral blood mononuclear cells (PBMC). MAb interaction with Env, lipids, and cells was determined by surface plasmon resonance (SPR), flow cytometry, and fluorescent microscopy. Results: No mAbs bound HIV-1 wild-type Envs by SPR and none significantly neutralized HIV-1 primary isolate pseudoviruses in the TZM/bl assay. In PBMC, β2-glycoprotein I-dependent mAbs minimally inhibited infection. In contrast, β2-glycoprotein I-independent anti-lipid mAbs (PGN632, P1, IS4, CL1) inhibited HIV-1 primary isolate infection of PBMC (IC80s <0.02 to 45 μg/mL). The most potent mAb PGN632 inhibited 7/7 B and C clade HIV-1 isolates (IC80s <0.02-0.16 μg/mL) and SHIV SP162P3 (IC80 0.06 μg/mL). Cell preincubation and virus capture studies showed the mAbs acted at host cell surfaces to inhibit HIV-1 infection. Immunofluorescence of CD4+ T cells showed the mAbs bound to lipid rafts. Conclusion: Anti-lipid human mAbs inhibit HIV-1 infection in vitro in PBMC likely by binding CD4+ T cell lipid rafts. Testing these mAbs in passive therapy trials in vivo in non-human primates will be important to determine their protective effect. Non-pathogenic anti-lipid antibodies may provide a target for HIV-1 vaccine development."
A summary of Tony Moody's presentation was given in the rapporteur session by Ralph Pantophlet shown here on pages 8 thru 13. In these slides the same mab is refered to be 11.31.
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