Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 12 3 2013 09 15 269 275 EN Fatemeh Ramezani Hepatitis B Molecular Laboratory, Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Mehdi Norouzi Hepatitis B Molecular Laboratory, Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Gholam Reza Sarizade Khoozestan Province Blood Trasfusion, Ahvaz, Iran Vahdat Poortahmasebi Hepatitis B Molecular Laboratory, Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Ebrahim Kalantar Gholhak Medical Laboratory, Tehran, Iran Lars Magnius Virological Department, Swedish Institute for Infectious Disease Control, Solna, Sweden Helen Norder Virological Department, Swedish Institute for Infectious Disease Control, Solna, Sweden Esteban Domingo Centro de Biología Molecular, Severo Ochoa, (CSIC-UAM), Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain Seyed Mohammad Jazayeri Hepatitis B Molecular Laboratory, Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran 2015 10 16 Mutations in the human hepatitis B virus (HBV) genome contribute to its escape from host immune surveillance and result in persistent infections. The aim of this study was to characterize the molecular variations of the surface gene and protein in chronically-infected patients from the southern part of Iran. The  surface  genes  from  12  HBV  chronic  carriers  were  amplified, sequenced  and subsequently aligned using international and national Iranian database. All strains belonged to genotype D, subgenotype D1 and subtype ayw2. Of all 30 muta-tions occurred at 22 nucleotide positions, 18 (60%) were missense (amino acid altering) and 12 (40%) were silent (no amino acid changing). The mean mutation frequency (missense to silent nucleotide ratio), was 1.5, indicating application of a high positive selection pressure on the surface proteins. At the amino acid level, of 17 substitutions, 15 (88%) occurred in different immune epitopes within surface protein, of which 7 (46.6%) in B cell epitopes in 5 residues; 7 (46.6%) in T helper epitopes in 6 positions; 1 (7%) in inside CTL epitopes in 1 residue. We therefore conclude that the distribution of 93.2% of amino acid mutations inside B and T helper immune epitopes as well as the ratio between silent and missense nucleotide mutations showed a positive, focused immune selection pressure on the surface protein, which led to the evolution and emergence of escape mutants in these patients. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/503 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/503/537