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Hepatitis B Virus Surface Antigen Variants Clustered Within Immune Epitopes in Chronic Hepatitis B Carriers From Hormozgan Province, South of Iran



Norouzi M1 ; Ghorashi SA1 ; Ataei B2 ; Yaran M2 ; Malekzadeh R3 ; Alavian SM4 ; Judaki MA5 ; Ghamari S5 ; Namazi A5 ; Rahimnia R5 ; Khedive A5 ; Jazayeri SM5
Authors
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Authors Affiliations
  1. 1. Iranian National Institute for Genetic Engineering and Biotechnology, Tehran, Iran
  2. 2. Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Digestive Disease Research Center, Shariati Hospital, Tehran, Iran
  4. 4. Baqiyatallah University of Medical Sciences, Baqiyatallah Research Centre for Gastroenterology and Liver Disease, Tehran, Iran
  5. 5. Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran

Source: Iranian Journal of Basic Medical Sciences Published:2010

Abstract

Objective(s): The aim of this study was to characterize the hepatitis B virus surface protein genotypes and sequence variations among hepatitis B virus surface antigen (HBsAg) positive chronic patients in Hormozgan province, south of Iran. Materials and Methods: A total of 8 patients enrolled in this study. The surface gene was amplified and directly sequenced. Genotypes and nucleotide/amino acid substitutions were identified compared to the sequences obtained from the database. Results: All strains belonged to genotype D. Overall 77 mutations occurred at 45 nucleotide positions, of them, 44 (57.14%) were silent (no amino acid altering) and 33 (42.86%) were missense (amino acid changing). A number of 24 (80%) out of 30 amino acid changes occurred in different immune epitopes within surface protein, of which, 9 (30%) in B cell epitopes in 7 residues (2 occurred in a determinant region); 8 (42.1%) in T helper epitopes in 7 residues and 7 (10%) in 4 residues inside CTL epitopes. Conclusion: Hepatitis B virus genome containing mutated immune epitopes no longer could be recognized by specific T-cells of the host immune surveillance and did not enhance anti-HBs production. This could led to the progression of chronicity of hepatitis B virus infection.
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