RESUMO
Post-transfusion hepatitis is still an important problem, despite the screening of blood donors for hepatitis B (HBV) and C virus infections. We assessed whether HBV DNA might be detected by PCR in prospectively collected serum samples of patients with unexplained post-transfusion hepatitis but no immunological HBV markers. We found HBV DNA in 4 (20%) of 20 patients with unexplained post-transfusion hepatitis and in 5 patients with mildly increased aminotransferases. The clinical course of these HBV infections was usually mild and self-limiting. Thus we found that low-titre, immunologically negative HBV infections do exist and might represent a significant cause of post-transfusion hepatitis.
Assuntos
Procedimentos Cirúrgicos Cardíacos , Hepatite B/imunologia , Hepatite B/transmissão , Reação Transfusional , Alanina Transaminase/sangue , Aspartato Aminotransferases/sangue , Sequência de Bases , DNA Viral/análise , Anticorpos Anti-Hepatite B/sangue , Antígenos de Superfície da Hepatite B/sangue , Vírus da Hepatite B/genética , Humanos , Dados de Sequência Molecular , Reação em Cadeia da Polimerase , Estudos ProspectivosRESUMO
It was previously demonstrated that the serum of some patients without immunological evidence of HBV infection contains the virus. Here we demonstrated by sequence analysis that the serum of such a patient contained a mixed HBV population. In comparison with HBV genomes of different genotypes twenty-two nucleotide variations were found in all clones sequenced in parallel. One nucleotide variation was identified within the enhancer I. Twelve of the twenty-two nucleotide variations caused altogether fifteen changes of amino acid sequence in known or predicted viral proteins. The proteins of the P open reading frame, which are most important for viral replication, were affected by nine amino acid substitutions. Three amino acid substitutions concerned the product of the X gene, a transcriptional transactivator of various viral and cellular promoters. Three mutations were only observed in some of the clones. One point mutation affected the direct repeats of the enhancer II. It occurred together with an 8 bp-deletion involving the C promoter region and the X gene. The third mutation was a single insertion, causing a fusion of the X and C gene. One or several of the identified mutations could be responsible for the diminished rate of replication and consequently for the low-titred, immunologically negative HBV infection.
