SIMILARITIES OF SPECIFICITY AND COFACTOR DEPENDENCE IN SERUM ANTIPHOSPHOLIPID ANTIBODIES FROM PATIENTS WITH HUMAN PARVOVIRUS B19 INFECTION AND FROM THOSE WITH SYSTEMIC LUPUS-ERYTHEMATOSUS

Citation
S. Loizou et al., SIMILARITIES OF SPECIFICITY AND COFACTOR DEPENDENCE IN SERUM ANTIPHOSPHOLIPID ANTIBODIES FROM PATIENTS WITH HUMAN PARVOVIRUS B19 INFECTION AND FROM THOSE WITH SYSTEMIC LUPUS-ERYTHEMATOSUS, Arthritis and rheumatism, 40(1), 1997, pp. 103-108
Citations number
15
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
00043591
Volume
40
Issue
1
Year of publication
1997
Pages
103 - 108
Database
ISI
SICI code
0004-3591(1997)40:1<103:SOSACD>2.0.ZU;2-N
Abstract
Objective. To assess the phospholipid specificity and immunoglobulin i sotype of antiphospholipid (aPL) antibodies in patients with acute par vovirus B19 infection. Methods. Specificity of aPL and isotype distrib ution in the negatively charged phospholipids, cardiolipin and phospha tidyl serine, and in the neutral phospholipid, phosphatidyl ethanolami ne, were measured in the sera of patients with acute parvovirus B19 in fections (n = 12), in those with other acute viral infections (n = 10) , and in those,vith syphilis (n = 15) by enzyme-linked immunosorbent a ssays, The dependence of anticardiolipin (aCL) binding on the presence of beta(2)-glycoprotein I (beta(2)-GPI) as a binding cofactor was ass essed in these same groups, and was compared with sera from systemic l upus erythematosus (SLE) patients (n = 11) with raised aCL antibody re activity. Results. Antibodies against any of the 3 phospholipids were found in all 3 groups of patients with infections (B19 in 11 of 12 pat ients, other viral infections in 8 of 10 patients, and syphilis in 14 of 15 patients), B19 patients' sera contained predominantly IgG antibo dies against the negatively charged phospholipids, cardiolipin and pho sphatidyl serine, and differed in their specificity and isotype distri bution from those found in the other 2 patient groups, B19-associated aCL increased their binding to antigen in the presence of beta(2)-GPI as a binding cofactor, similar to aCL found in SLE patients, but unlik e antibodies from patients with other viral infections or from those w ith syphilis. Conclusion. The results show the remarkable similarity i n specificity of aPL antibodies between B19-infected patients and SLE patients, and raise the question of whether parvovirus infection may b e a trigger for the development of aPL antibodies in autoimmune diseas es.