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Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Scopus, Emerging Sources Citation Index
Online ISSN 1827-1642
Sayad B. 1, Anvari F. A. 2, Alavian S. M. 3, Norouzi M. 2, Hamzelooie M. 1, Shirvani M. 1, Pourhoseingholi A. 4, Khedive A. 2, Ghamari S. 2, Judaki M. A. 2, Jazayeri S. M. 2
1 Kermanshah Liver Diseases and Hepatitis Reseaerch Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
2 Hepatitis B Molecular Laboratory, Department of Virology-School of Public Health Tehran University of Medical Sciences, Tehran, Iran
3 Baqiyatallah Research Centre for Gastroenterology and Liver Disease, Baqiyatallah University of Medical Sciences, Tehran, Iran
4 Research Center for Gastroenterology and Liver diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AIM: Hepatitis B virus (HBV) genetic and protein variations have been found in chronic HBV infected patients who did not receive any treatment and active or passive immunizations. The aims of this study were to determine the genotypes as well as the patterns of variations distribution in chronically infected patients from the west part of Iran.
METHODS:Forty-six people with chronic HBV infection were enrolled in the study. The surface genes were amplified, sequenced and subsequently aligned using international and national Iranian database.
RESULTS: All strains belonged to genotype D, subgenotype D1 and subtype ayw2. Of all 116 “mutations” that occurred at 59 nucleotide positions, 49 (42.2 %) were missense (amino acid altering) and 67 (57.7%) were silent (no amino acid changing), respectively. At the amino acid level, 38 (79.1%) out of 48 amino acid mutations occurred in different immune epitopes within the surface proteins, of which 2 (5.2%) occurred in B cell; 12 (31.5%) in T helper and 24 (63.1%) inside CTL epitopes. There were significant associations between amino acid mutations (especially within immune epitopes) and anti-HBe positivity and increased ALT levels (P values: 0.014 and 0.04, respectively).
CONCLUSION: The distribution of amino acid mutations as well as the ratio between silent and missense nucleotide mutations showed that a narrowly focused immune pressure had already been on the surface protein T cell epitopes (94.9% of mutations), particularly CTL epitopes which led to the emergence of escape mutants in these patients.