HBsAg Mutants Clustered Mainly Outside of “a” Determinant in Chronic Carriers From Azarbayjan Province, Iran

Sajad Shahmoradi; Mohammad Hossein Somi; Mehdi Norouzi; Seyed Moayed Alavian; Hadi Karimzadeh; Ramin Rahimnia; Alireza Namazi; Abolfazl Khedive; seyed Mohammad Jazayeri

Jundishapur Journal of Microbiology

Ahvaz Jundishapur University of Medical Sciences

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HBsAg Mutants Clustered Mainly Outside of “a” Determinant in Chronic Carriers From Azarbayjan Province, Iran

Author(s):

Sajad Shahmoradi¹,

Mohammad Hossein Somi²,

Mehdi Norouzi¹,

Seyed Moayed Alavian³,

Hadi Karimzadeh¹,

Ramin Rahimnia¹,

Alireza Namazi¹,

Abolfazl Khedive¹,

seyed Mohammad Jazayeri^1,*

1Hepatitis B Molecular Laboratory, Department of Virology-School of Public Health, Tehran University of Medical Sciences, Tehran, IR Iran

2Liver and Gastrointestinal Disease Research Center, Eastern Azarbyjan University of Medical Sciences, Tabriz, IR Iran

3Baqiyatallah University of Medical Sciences, Baqiyatallah Research Center for Gastroenterology and Liver Disease, Tehran, IR Iran

Jundishapur Journal of Microbiology:Vol. 6, issue 6; e94138

Published online:Aug 10, 2013

Article type:Research Article

Received:May 21, 2019

Accepted:May 30, 2012

How to Cite:Sajad ShahmoradiMohammad Hossein SomiMehdi NorouziSeyed Moayed AlavianHadi KarimzadehRamin RahimniaAlireza NamaziAbolfazl Khediveseyed Mohammad Jazayeriet al.HBsAg Mutants Clustered Mainly Outside of “a” Determinant in Chronic Carriers From Azarbayjan Province, Iran.Jundishapur J Microbiol.6(6):e94138.

Abstract

Background: Hepatitis B virus (HBV) genetic and protein variations have been observed in chronic patients frequently. However, their role in the pathogenesis of chronicity has not been explored yet.

Objectives: The aims of this study were to determine the genotypes as well as the patterns of variations distribution in chronically infected patients from the north western part of Iran.

Materials and Methods: The surface genes from 17 chronic carriers 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 56 “mutations” that occurred at 37 nucleotide positions, 25 (44.6%) were missense (amino acid altering) and 31 (55.4%) were silent (no amino acid changing) (S/M ratio: 1.2). At the amino acid level, 21 (91.3%) out of 23 amino acid mutations occurred in different immune epitopes within the surface proteins, of which 3 (14.3%) occurred in B cell, 8 (38%) in T helper and 10 (47.7%) inside CTL epitopes. In general, the association between amino acid mutations and especially, immune epitope substitutions was more significant in terms of HBeAg status than ALT levels in patients.

Conclusions: The distribution of amino acid mutations as well as the ratio between missense and silent nucleotide mutations (dN/dS) showed that a narrowly focused immune pressure had already been on the surface protein (especially CTL epitopes) which led to the emergence of escape mutants in these patients who were in tolerance phase of chronicity.

Keywords

HBV Genotype D

HBsAg variants

HBsAg Epitopes Mutations

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