title: Clinical and serological variation between patients infected with different Hepatitis B virus genotypes.
abstract: Hepatitis B virus (HBV) has eight genotypes which have distinct geographical distributions. Studies comparing differences in the clinical outcomes of infections caused by strains with genotype-related variations in the HBV genome have largely compared genotypes B and C and genotypes A and D but not all four genotypes. The present study included 196 HBV-infected patients attending an infectious diseases outpatient clinic in Sweden. The age and geographic origin, liver function, HBeAg and anti-HBe status, and the presence or absence of HBV DNA were analyzed for each patient. HBV DNA was detected in 144 patients, and the HBV genotype and the core promoter and precore sequences were determined for the isolates from 101 of these patients. Among the patients who might be considered most likely to be nonviremic, namely, anti-HBe-positive HBV carriers with normal alanine aminotransferase (ALT) levels, 65% had detectable HBV DNA and were thus viremic. Among the viremic patients, HBeAg-positive patients were more likely to have elevated ALT levels than anti-HBe-positive patients. HBV genotypes A to F were represented in the study, and their distributions coincided accurately with the origin of the patient. A significantly higher number of genotype D-infected patients were anti-HBe positive and had elevated ALT levels (42% of genotype D-infected patients but 0% of patients infected with genotypes B and C). Genotype D strains with mutations in the core promoter and precore regions were significantly correlated with elevated ALT levels in the patients. The differences were not age related. Therefore, in this large-scale cross-sectional study, genotype D appears to be associated with more active disease.
authors.affiliation: Division of Infectious Diseases, Department of Medical Microbiology, Dermatology and Infection, Lund University, SE-221 85 Lund, Sweden. Karin.Kidd@infek.lu.se
authors.forename: Karin
authors.initials: K
authors.lastname: Kidd-Ljunggren
authors.forename: Erling
authors.initials: E
authors.lastname: Myhre
authors.forename: Jonas
authors.initials: J
authors.lastname: Bläckberg
mesh_terms: D000328:Adult; D000349:Africa; D001208:Asia; D002489:Central America; D004279:DNA, Viral / Q000097:blood; D005060:Europe; D005260:Female; D005838:Genotype; D006509:Hepatitis B / Q000453:epidemiology / Q000503:physiopathology* / Q000821:virology; D006510:Hepatitis B Antibodies / Q000097:blood*; D006513:Hepatitis B e Antigens / Q000097:blood* / Q000276:immunology; D006515:Hepatitis B virus / Q000145:classification* / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D008111:Liver Function Tests; D008297:Male
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006513:Hepatitis B e Antigens