Increased prevalence of anti-phospholipid antibodies (aPL) and increased levels of lipid peroxidation have been described in patients with HIV infection. To assess the binding specificity and avidity or aPL antibodies in HIV infection, sera from 44 HIV-1 infected patients were evaluated for antibodies td cardiolipin (aCL), phosphatidyl serine (aPS), phosphatidyl inositol (aPI) and phosphatidyl choline (aPC) using enzyme linked immunosorbent assay (ELISA) methods, Sera from 30 patients with systemic-lupus erythematosus (SLE), but without features of anti-phospholipid syndrome (APS) (SLE/non APS); six with SLE and secondary APS, (SLE/APS) and 11 with primary APS (PAPS) were also evaluated as controls. The resistance of the aPL antibody binding to dissociating agents was evaluated by treating the ELISA wells, after serum incubation with 2M urea-or 0.6 M NaCl for 10 min. An anti-beta 2-glycoprotein-I (beta 2-GPI) ELISA was used to assess serum reactivity against beta 2-GPI, a plasma protein considered as the true antigen of aCL antibodies occurring in APS and SLE patients, The prevalence of aCL, aPS, aPI and aPC antibodies in HIV-1 infection was 36%, 56%, 34% and 43% respectively, which was:comparable to that found in SLE/APS and PAPS,patients and significantly higher than that observed in SLE/non-APS patients. Anti-beta 2-GPI antibodies occurred in 5% of HIV-1 infected vs. 17% in SLE/non-APS (P=0.11), 50% in SLE/APS (P = 0.009) and 70% in PAPS patients (P = 0.0014). A significant decrease of aPL binding after urea and NaCl treatment was observed in the sera of HIV-1-infected, compared to that of APS patients, indicating that aPL antibodies from HIV-1 infected individuals have low resistance to dissociating agents. Ln conclusion, aPL antibodies (1) occur in HIV-1 infection; (2)tend-to recognize various phospholipids but not beta 2-GPI; and (3) are of low resistance to dissociating agents-a finding probably reflecting low antibody avidity. Finally, these, like the autoimmune-type aCL antibodies, tend to recognize the oxidized CL-a finding probably indicating autoantibody generation as a result of neoepitope formation by oxidized PLs; (C) 1999 Academic Press.
