Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B

2012 ◽  
Vol 84 (11) ◽  
pp. 1719-1726 ◽  
Author(s):  
Rim Ouneissa ◽  
Olfa Bahri ◽  
Nissaf Ben Alaya-Bouafif ◽  
Sofiene Chouaieb ◽  
Ahlem Ben Yahia ◽  
...  
2008 ◽  
Vol 15 (10) ◽  
pp. 753-760 ◽  
Author(s):  
H. Poustchi ◽  
A. Mohamadkhani ◽  
S. Bowden ◽  
G. Montazeri ◽  
A. Ayres ◽  
...  

2012 ◽  
Vol 56 ◽  
pp. S194
Author(s):  
S.Y. Yim ◽  
S.H. Um ◽  
J.D. Kim ◽  
J.Y. Jung ◽  
C.H. Kim ◽  
...  

2008 ◽  
Vol 43 (7) ◽  
pp. 558-564 ◽  
Author(s):  
Kazuhiko Hayashi ◽  
Yoshiaki Katano ◽  
Yasushi Takeda ◽  
Takashi Honda ◽  
Masatoshi Ishigami ◽  
...  

2000 ◽  
Vol 38 (8) ◽  
pp. 2975-2981 ◽  
Author(s):  
Nicola Petrosillo ◽  
Giuseppe Ippolito ◽  
Laura Solforosi ◽  
Pietro E. Varaldo ◽  
Massimo Clementi ◽  
...  

A nosocomial outbreak of hepatitis B occurred among the inpatients of a hematology unit. Nine of the 11 infected patients died from fulminant hepatitis. An investigation was conducted to identify the source of infection and the route of transmission. Two clusters of nosocomial hepatitis B were identified. The hepatitis B virus (HBV) genome from serum samples of all case patients, of one HBsAg-positive patient with acute reactivation of the infection, and of eight acutely infected, unrelated cases was identified by PCR amplification of viral DNA and was entirely sequenced. Transmission was probably associated with breaks in infection control practices, which occurred as single events from common sources or through a patient-to-patient route, likely the result of shared medications or supplies. Sequence analysis evidenced close homology among the strains from the case patients and that from the patient with reactivation, who was the likely source of infection. Molecular analysis of viral isolates evidenced an accumulation of mutations in the core promoter/precore region, as well as several nucleotide substitutions throughout the genome. The sequences of all patients were compared with published sequences from fulminant and nonfulminant HBV infections.


2005 ◽  
Vol 12 (2) ◽  
pp. 160-167 ◽  
Author(s):  
L. H. Song ◽  
D. N. Duy ◽  
V. Q. Binh ◽  
A. J. F. Luty ◽  
P. G. Kremsner ◽  
...  

Author(s):  
Israr Ahmad ◽  
Kafeel Ahmad

Abstract Objective: The aim of this study was to analyze mutations in precore/core promoter region of HBV genome in chronic hepatitis B patients from three cities of Pakistan. Methods: A total of 50 treatment naïve chronic hepatitis B patients from Pakistan were selected. Viral load, HBeAg/antiHBe status, HBV ELISA and ALT levels were determined. Direct sequencing of BCP and PC region of HBV genome was carried out following a nested PCR approach. Phylogenetic tree was constructed using MEGA software version 6.0.  Statistical analysis was carried out using SPSS version 16.0. Results: The G1896A precore stop codon mutation was detected in 19 (38%) isolates. The mutation was present in 17(34%) isolates from HBeAg negative patients and 2(4%) isolates from HBeAg positive patients. The Classic A1762T/G1764A double mutation was noted in 15 (30%) isolates. Mutation at position 1764 was observed in 12 (48%) samples. A rare G1764T mutation was also detected in 6 (12%) isolates. The CG1802-1803 mutation was detected in 47(94%) isolates. The T1858 mutation was detected in all 50 (100%) isolates. The GCAC Kozak sequence was present in 43(86%) isolates. The CAA1817-1819 mutation was observed in 49(98%) isolates and G1888 mutation was detected in 49(98%) isolates. Overall, 9(18%) isolates had wild-type sequences at all important loci including positions 1762,1764 and 1896. The pattern of sequences at genotype specific positions and phylogenetic tree revealed that majority of study isolates belonged to genotype D. Conclusions: Sequences results showed that precore region was comparatively more conserved than BCP region. Continuous...  


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