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Identification of Hepatitis B Virus Surface Antigen (Hbsag) Genotypes and Variations in Chronic Carriers From Isfahan Province, Iran



Norouzi M1 ; Ghorashi SA1 ; Abedi F2 ; Nejatizadeh A2 ; Ataei B3 ; Malekzadeh R4 ; Alavian SM5 ; Judaki MA6 ; Ghamari S6 ; Namazi A6 ; Rahimnia R6 ; Khedive A6 ; Jazayeri SM6
Authors
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Authors Affiliations
  1. 1. Iranian National Institute for Genetic Engineering and Biotechnology, Tehran, Iran
  2. 2. Research center for infectious diseases and tropical medicine, School of Medicine, Hormozgan University of Medical Sciences, Iran
  3. 3. Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Digestive Disease Research Center, Shariati Hospital, Tehran, Iran
  5. 5. Baqiyatallah University of Medical Sciences, Baqiyatallah Research Centre for Gastroenterology and Liver Disease, Tehran, Iran
  6. 6. Hepatitis B Molecular Laboratory, Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran

Source: Iranian Journal of Public Health Published:2012

Abstract

Background: Hepatitis B virus (HBV) gene and protein variations are frequently been seen in chronic patients. The aims of study were to determine the genotypes as well as the patterns of variations distribution in chronically-infected patients from the central part of Iran. Methods: The surface gene was 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 62 mutations occurred at 39 nucleotide positions, 31 (50%) were missense (amino acid altering) and 31 (50%) were silent (no amino acid changing). At the amino acid level, 30 substitutions occurred, however, 3 were in positions 122 and 127, corresponded to subtypic determination. 22 (73%) out of 30 amino acid mutations occurred in different immune epitopes within surface protein, of which 12 (54.54%) in B cell epitopes in 10 residues; 5 (45.45%) in T helper epitopes in positions; 5 (22.73%) in inside CTL epitopes in 4 residues. Conclusion: The distribution of amino acid mutations as well as the ratio between silent and missense nucleotide mutations showed a narrowly focused immune pressure had already been on the surface protein in these patients, led to the emergence of escape mutants in these patients.
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