Molecular epidemiology of hepatitis B virus in Dakar, Sénégal
Using DNA chip technology and real‐time quantitative PCR, molecular profile of HBV strains infecting blood donors and patients in Dakar, Sénégal was studied. All HBsAg‐positive blood donors (n = 175) and all patients who presented with chronic hepatitis B (n = 29) between 1st June 2003 and 31st July...
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Veröffentlicht in: | Journal of medical virology 2006-03, Vol.78 (3), p.329-334 |
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Sprache: | eng |
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Zusammenfassung: | Using DNA chip technology and real‐time quantitative PCR, molecular profile of HBV strains infecting blood donors and patients in Dakar, Sénégal was studied. All HBsAg‐positive blood donors (n = 175) and all patients who presented with chronic hepatitis B (n = 29) between 1st June 2003 and 31st July 2003 were studied. One patient, a blood donor, was coinfected by HCV, and nine patients had anti‐HDV antibodies. Few persons in either group were HBeAg‐positive. Viral load values were relatively low but correlated with biochemical abnormalities. Patients were infected mainly by genotype E (72%). Patients infected by genotype A (28%) tended to be younger than other patients. There was no significant difference between the blood donors and the patients with hepatitis B as regards virological markers, including viral load, when the HBV genotype was taken into account. The BCP A1762T and G1764A mutations were found in four patients and one patient, respectively; the two mutations were never found in the same patient. The W28* mutation at position 1896 of the core was detected in 19 of the 32 genotyped patients, 18 (83%) of whom had genotype E infection. ALT levels were not influenced by HBV mutations. This study shows a low frequency of clinical signs in HBsAg‐positive blood donors, a relatively low level of viral replication, and a high frequency of pre‐core mutants in this West African population. These results underline the importance of molecular characterization of HBV infection as specific treatments become available in this region. J. Med. Virol. 78:329–334, 2006. © 2006 Wiley‐Liss, Inc. |
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ISSN: | 0146-6615 1096-9071 |
DOI: | 10.1002/jmv.20544 |