Extended report
Cofactor dependence and isotype distribution of anticardiolipin
antibodies in viral infections
H Guglielmonea b, S Vitozzia, O Elbarchaa, E Fernandeza
a Laboratorio de
Análisis Clínicos Especializados (LACE), Córdoba, Argentina, b Departamento de Bioquímica
Clínica, Facultad de Ciencias Químicas, Universidad Nacional de
Córdoba, Argentina
Correspondence to: Dr Guglielmone, Laboratorio de Análisis Clínicos Especializados (LACE), Av Velez Sarsfield 562-4to Piso, (5000) Córdoba, Argentina hgugli{at}bioclin.fcq.unc.edu.ar
Accepted for publication 12 September
2000
BACKGROUND
Antibodies
to cardiolipin (aCLs) are often detected in patients with autoimmune
disorders or infectious diseases.
OBJECTIVE
To
investigate the distribution of aCL isotypes and requirement of protein
cofactor in viral infections in order to establish the importance, if
any, of these antibodies in these infectious diseases.
PATIENTS AND
METHODS
The isotype distribution of aCLs in the
sera from 160 patients with infection caused by HIV-1 (n=40), hepatitis
A virus (n=40), hepatitis B virus (n=40), or hepatitis C virus (n=40)
was studied by standardised enzyme linked immunosorbent assay (ELISA)
in the presence and absence of protein cofactor (mainly
2-glycoprotein I). Serum samples from healthy volunteers and
patients with syphilis and antiphospholipid syndrome were also included
and served as negative and positive control groups respectively.
RESULTS
The prevalence
of one or more aCL isotypes in serum of patients with HIV-1, hepatitis
A virus, hepatitis B virus, or hepatitis C virus infection was 47%,
92%, 42%, and 17% respectively (principally IgM and/or IgA). Most of
these antibodies were mainly cofactor independent.
CONCLUSIONS
The
presence of aCLs in viral infections is principally cofactor
independent, suggesting that cofactor dependence of the aCLs should be
assessed to distinguish subjects most likely to suffer from clinical
symptoms observed in the presence of these antibodies.
© 2001 by Annals of the Rheumatic Diseases
This article has been cited by other articles:
-
Levy, Y, Almog, O, Gorshtein, A, Shoenfeld, Y
(2006). The environment and antiphospholipid syndrome. Lupus
15: 784-790
[Abstract] -
Ozturk, M. A., Haznedaroglu, I. C., Turgut, M., Goker, H.
(2004). Current Debates in Antiphospholipid Syndrome: The Acquired Antibody-Mediated Thrombophilia. CLIN APPL THROMB HEMOST
10: 89-126
[Abstract] -
Loizou, S, Singh, S, Wypkema, E, Asherson, R A
(2003). Anticardiolipin, anti-{beta}2-glycoprotein I and antiprothrombin antibodies in black South African patients with infectious disease. Ann Rheum Dis
62: 1106-1111
[Abstract] [Full Text] -
Lieby, P., Soley, A., Knapp, A.-M., Cerutti, M., Freyssinet, J.-M., Pasquali, J.-L., Martin, T.
(2003). Memory B cells producing somatically mutated antiphospholipid antibodies are present in healthy individuals. Blood
102: 2459-2465
[Abstract] [Full Text]
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
