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Journal of Clinical Microbiology, November 2004, p. 5121-5124, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5121-5124.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Diagnostic Relevance of Immunoglobulin G Avidity for Hepatitis A Virus

Anne-Marie Roque-Afonso,1 Liliane Grangeot-Keros,2 Bénédicte Roquebert,1 Delphine Desbois,1 Jean-Dominique Poveda,3 Vincent Mackiewicz,1 and Elisabeth Dussaix1*

Centre National de Référence pour les Virus à Transmission Entérique, Laboratoire de Virologie, Hôpital Paul Brousse, Villejuif,1 Laboratoire de Virologie, Hôpital Antoine Béclère, Clamart,2 Laboratoire Pasteur Cerba, Cergy Pontoise, France3

Received 8 March 2004/ Returned for modification 8 May 2004/ Accepted 18 July 2004

Diagnosis of acute hepatitis A virus (HAV) infection is based on the detection of HAV immunoglobulin M (IgM). However, IgM could be detected due to nonspecific polyclonal activation of the immune system. An avidity test for anti-HAV IgG was developed to distinguish acute infection, where low-avidity antibodies are detected, from immune reactivation. The assay was tested on 104 samples, including 11 sera from patients with past infection, 15 sera from patients with acute infection and 4 collected after recovery, 10 sera from vaccinated subjects, 4 sera from patients with suspected immune reactivation, and 60 unselected HAV-IgM positive sera, collected over 1 year in a routine laboratory. The avidity index (AI) was expressed as percentage. The results were provided as the mean ± one standard deviation. Patients with a history of prior infection had AIs of >70% (mean, 86% ± 10), whereas the mean AI was 36% ± 16 during acute HAV infection (P < 0.001). Within the first month after the onset of hepatitis, avidity was either noncalculable due to a very low IgG titer or <50%. In patients with immune reactivation, avidity was >70% (88% ± 10%), a finding consistent with a prior infection. Among the 60 unselected sera, 35 (58%) had a noncalculable or <50% avidity, and most of them had a detectable HAV RNA, confirming HAV infection. In contrast, 16 (27%) had an avidity of >70%, and none was reverse transcription-PCR positive, suggesting immune reactivation. These 16 patients were significantly older than the others (50 ± 16 years versus 26 ± 14 years). The new anti-HAV IgG avidity assay we developed could improve HAV infection diagnosis, particularly in elderly patients.

* Corresponding author. Mailing address: Laboratoire de Virologie, Hôpital Paul Brousse, 12 Ave. Paul Vaillant-Couturier, 94804 Villejuif, France. Phone: (33) 1-45593720. Fax: (33) 1-45593724. E-mail: elisabeth.dussaix{at}pbr.ap-hop-paris.fr.

Journal of Clinical Microbiology, November 2004, p. 5121-5124, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5121-5124.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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