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