title: Molecular epidemiology of hepatitis B virus in Dakar, Sénégal.
abstract: 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.
authors.affiliation: Unité d'Epidémiologie des Maladies Emergentes, Institut Pasteur, Paris, France. vray@pasteur.fr
authors.forename: Muriel
authors.initials: M
authors.lastname: Vray
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Debonne
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Sire
authors.forename: Nathalie
authors.initials: N
authors.lastname: Tran
authors.forename: Benoit
authors.initials: B
authors.lastname: Chevalier
authors.forename: Jean-Christophe
authors.initials: JC
authors.lastname: Plantier
authors.forename: Fatou
authors.initials: F
authors.lastname: Fall
authors.forename: Guy
authors.initials: G
authors.lastname: Vernet
authors.forename: François
authors.initials: F
authors.lastname: Simon
authors.forename: Papa Saliou
authors.initials: PS
authors.lastname: Mb
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001782:Blood Donors; D018389:Codon, Nonsense; D004279:DNA, Viral / Q000235:genetics; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000302:isolation & purification; D006509:Hepatitis B / Q000150:complications / Q000453:epidemiology / Q000821:virology*; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006513:Hepatitis B e Antigens / Q000032:analysis; D006515:Hepatitis B virus / Q000145:classification* / Q000235:genetics* / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000150:complications / Q000453:epidemiology / Q000821:virology; D006526:Hepatitis C / Q000150:complications; D003699:Hepatitis D / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D017720:Molecular Epidemiology; D020411:Oligonucleotide Array Sequence Analysis; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D012675:Senegal / Q000453:epidemiology; D019562:Viral Load
chemical_list: D018389:Codon, Nonsense; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D000410:Alanine Transaminase