PMID- 10550222 OWN - NLM STAT- MEDLINE DCOM- 20000229 LR - 20151119 IS - 0896-8411 (Print) IS - 0896-8411 (Linking) VI - 13 IP - 3 DP - 1999 Nov TI - Anti-phospholipid antibodies in HIV infection and SLE with or without anti-phospholipid syndrome: comparisons of phospholipid specificity, avidity and reactivity with beta2-GPI. PG - 347-55 AB - 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. CI - Copyright 1999 Academic Press. FAU - Petrovas, C AU - Petrovas C AD - Department of Pathophysiology, Medical School, National University of Athens, Athens, Greece. FAU - Vlachoyiannopoulos, P G AU - Vlachoyiannopoulos PG FAU - Kordossis, T AU - Kordossis T FAU - Moutsopoulos, H M AU - Moutsopoulos HM LA - eng PT - Comparative Study PT - Journal Article PL - England TA - J Autoimmun JT - Journal of autoimmunity JID - 8812164 RN - 0 (Anti-HIV Agents) RN - 0 (Antibodies, Anticardiolipin) RN - 0 (Cardiolipins) RN - 0 (Glycoproteins) RN - 0 (Phospholipids) RN - 0 (Reverse Transcriptase Inhibitors) RN - 0 (beta 2-Glycoprotein I) RN - 451W47IQ8X (Sodium Chloride) RN - 8W8T17847W (Urea) SB - IM MH - Adult MH - Anti-HIV Agents/therapeutic use MH - Antibodies, Anticardiolipin/immunology MH - Antibody Affinity/*immunology MH - Antibody Specificity/*immunology MH - Antiphospholipid Syndrome/complications/*immunology MH - Cardiolipins/immunology MH - Female MH - Glycoproteins/*immunology MH - HIV Infections/drug therapy/*immunology MH - Hepatitis C/complications/immunology MH - Humans MH - Lupus Erythematosus, Systemic/complications/*immunology MH - Male MH - Phospholipids/*immunology MH - Pneumonia, Pneumocystis/complications/immunology MH - Reverse Transcriptase Inhibitors/therapeutic use MH - Sodium Chloride/immunology MH - Urea/immunology MH - beta 2-Glycoprotein I EDAT- 1999/11/07 09:00 MHDA- 2000/03/04 09:00 CRDT- 1999/11/07 09:00 PHST- 1999/11/07 09:00 [pubmed] PHST- 2000/03/04 09:00 [medline] PHST- 1999/11/07 09:00 [entrez] AID - S0896-8411(99)90324-4 [pii] AID - 10.1006/jaut.1999.0324 [doi] PST - ppublish SO - J Autoimmun. 1999 Nov;13(3):347-55. doi: 10.1006/jaut.1999.0324.