title: Hepatitis B virus genotypes and precore/core-promoter mutations in Tunisian patients with chronic hepatitis B virus infection.
abstract: OBJECTIVE
  The aim of this study was to determine the frequency of genotype and precore/core-promoter mutations in chronic hepatitis B virus (HBV) infected individuals in Tunisia.
  
  
  METHODS
  We studied 164 Tunisian patients (38 HBeAg-positive and 126 HBeAg-negative) with chronic HBV infection. Genotypes and precore/core-promoter mutations were studied using Inno-LiPA and Multiplex-PCR and PCR-RFLP methodology.
  
  
  RESULTS
  Alanine aminotransferase (ALT) levels were higher in HBeAg-positive compared with HBeAg-negative patients (p<0.05). Patients with HBeAg-positive chronic hepatitis B were younger than HBeAg-negative chronic hepatitis B patients. The 164 genotypes were distributed as follows: 1 genotype A (0.6%), 1 genotype B (0.6%), 3 genotype C (1.82%), 139 genotype D (84.75%), and 20 mixed genotypes (12.2%). In the precore region (41.5%) of the patients had exclusively PC mutant and (50.9%) had a mixture of wild-type and variant sequences. PC variant was more commonly found in HBeAg-negative patients than in HBeAg-positive patients (94.5% vs. 87.8%), respectively. The mutations in the core promoter were more common in HBeAg-negative patients (65.4%) than in HbeAg-positive patients (18.2%). These results indicate that genotype D is predominant in Tunisia. Precore mutation occurred invariably among HBeAg-positive and HBeAg-negative patients, whereas core-promoter mutations were more frequently found in HBeAg-negative patients.
  
  
  CONCLUSIONS
  Analysis of these mutants may prove useful for clinical evaluation and choice of therapy.
authors.affiliation: Immunology Laboratory, Charles Nicolle Hospital, Boulevard 9 Avril, 1006 Tunis, Tunisia. khaled.ayed@rns.tn <khaled.ayed@rns.tn>
authors.forename: Khaled
authors.initials: K
authors.lastname: Ayed
authors.forename: Yousr
authors.initials: Y
authors.lastname: Gorgi
authors.forename: Saloua
authors.initials: S
authors.lastname: Ayed-Jendoubi
authors.forename: Houda
authors.initials: H
authors.lastname: Aouadi
authors.forename: Imen
authors.initials: I
authors.lastname: Sfar
authors.forename: Tawfik
authors.initials: T
authors.lastname: Najjar
authors.forename: Taieb
authors.initials: T
authors.lastname: Ben Abdallah
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000410:Alanine Transaminase / Q000097:blood; D002648:Child; D004279:DNA, Viral / Q000235:genetics; D005260:Female; D005838:Genotype; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000145:classification* / Q000235:genetics* / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011401:Promoter Regions, Genetic; D014416:Tunisia
chemical_list: D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D000410:Alanine Transaminase