title: Anti-phospholipid antibodies in HIV infection and SLE with or without anti-phospholipid syndrome: comparisons of phospholipid specificity, avidity and reactivity with beta2-GPI.
abstract: 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 of aPL antibodies in HIV infection, sera from 44 HIV-1 infected patients were evaluated for antibodies to 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 2 M urea or 0.6 M NaCl for 10 min. An anti-beta2-glycoprotein-I (beta2-GPI) ELISA was used to assess serum reactivity against beta2-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-beta2-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. In conclusion, aPL antibodies (1) occur in HIV-1 infection; (2) tend to recognize various phospholipids but not beta2-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.
authors.affiliation: Department of Pathophysiology, Medical School, National University of Athens, Athens, Greece.
authors.forename: C
authors.initials: C
authors.lastname: Petrovas
authors.forename: P G
authors.initials: PG
authors.lastname: Vlachoyiannopoulos
authors.forename: T
authors.initials: T
authors.lastname: Kordossis
authors.forename: H M
authors.initials: HM
authors.lastname: Moutsopoulos
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use; D017153:Antibodies, Anticardiolipin / Q000276:immunology; D000915:Antibody Affinity / Q000276:immunology*; D000918:Antibody Specificity / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000276:immunology*; D002308:Cardiolipins / Q000276:immunology; D005260:Female; D006023:Glycoproteins / Q000276:immunology*; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology*; D006526:Hepatitis C / Q000150:complications / Q000276:immunology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology*; D008297:Male; D010743:Phospholipids / Q000276:immunology*; D011020:Pneumonia, Pneumocystis / Q000150:complications / Q000276:immunology; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D012965:Sodium Chloride / Q000276:immunology; D014508:Urea / Q000276:immunology; D053482:beta 2-Glycoprotein I
chemical_list: D019380:Anti-HIV Agents; D017153:Antibodies, Anticardiolipin; D002308:Cardiolipins; D006023:Glycoproteins; D010743:Phospholipids; D018894:Reverse Transcriptase Inhibitors; D053482:beta 2-Glycoprotein I; D012965:Sodium Chloride; D014508:Urea