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Journal of Clinical Microbiology, November 2004, p. 5015-5021, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5015-5021.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Strong Association between Genotype F and Hepatitis B Virus (HBV) e Antigen-Negative Variants among HBV-Infected Argentinean Blood Donors

Paulo H. C. França,1,2,3 Jorge E. González,4 M. Silvina Munné,4 Larissa H. Brandão,5 Vera S. Gouvea,1 Erwin Sablon,6 and Bart O. M. Vanderborght2,5,6*

Departamento de Virologia, Instituto de Microbiologia,1 Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro,2 Instituto de Diagnóstico Molecular Theranostica, Rio de Janeiro,5 Universidade da Região de Joinville, Joinville, Brazil,3 Laboratorio Nacional de Referencia, INEI, ANLIS-Dr. C. G. Malbrán, Buenos Aires, Argentina,4 Innogenetics NV, Ghent, Belgium6

Received 25 March 2004/ Returned for modification 22 June 2004/ Accepted 21 July 2004

A number of reports have indicated an increased risk of cirrhosis and hepatocellular carcinoma in hepatitis B virus (HBV)-infected individuals carrying HBV e antigen (HBeAg)-negative variants. Although distinct core promoter and precore mutations distributed according to geographical locality and viral genotype have been reported, epidemiological data from South America are still scarce. The prevalences of HBV genotypes and core promoter and precore polymorphisms in 75 HBeAg-negative Argentinean blood donors were surveyed. The observed frequencies of HBV genotypes were 64.0% for genotype F, 17.3% each for genotypes A and D, and 1.3% for genotype C. Genotype F strains were widely distributed and significantly more prevalent in the northern region of the country (P < 0.001). An overall high proportion of a stop codon mutation (UAG) at precore codon 28 (66.7%) was observed. Wild-type codon 28 (UGG) was present in 29.3% of the samples, and the remaining 4.0% of samples had mixed variants. The combination of A at nucleotide (nt) 1762 and G at nt 1764 of the core promoter was found in 58.7% of the samples. The variant profiles—T at nt 1762 and A at nt 1764 or A at nt 1762 and A at nt 1764—were detected in 28.0 and 1.3% of the samples, respectively. The observed core promoter polymorphisms could not be related to the ratio of HBeAg to anti-HBeAg antibody, HBV genotype, or precore codon 28 status. Nevertheless, a clear association of genotype F and a precore stop codon mutation was found (P < 0.05). In conclusion, HBV genotype F and mutant codon 28 strains predominated and were strongly associated in a geographically broad Argentinean blood donor population.

* Corresponding author. Mailing address: Instituto de Diagnóstico Molecular Theranostica, Caminho Rodrigo da Silva, 88, Alto da Boa Vista, Rio de Janeiro, Rio de Janeiro, CEP 20531-560 Brazil. Phone: 00 55 21 2483 1403. Fax: 00 55 21 2483 1403. E-mail: bvdb{at}alternex.com.br.

Journal of Clinical Microbiology, November 2004, p. 5015-5021, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5015-5021.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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