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Hepatitis B virus genotypes and hepatitis B surface antigen mutations in family contacts of hepatitis B virus infected patients with occult hepatitis B virus infection
Author(s) -
Kumar Gollapudi Tarun,
Kazim Syed Naqui,
Kumar Manoj,
Hissar Syed,
Chauhan Ranjit,
Basir Seemi Farhat,
Sarin Shiv Kumar
Publication year - 2009
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2008.05727.x
Subject(s) - hbsag , genotype , hepatitis b virus , medicine , virology , genotyping , virus , hepatitis b , gene mutation , hbeag , orthohepadnavirus , immunology , mutation , gene , biology , genetics
Background: The association and profile of surface gene mutations with viral genotypes have been studied in patients with chronic hepatitis B virus (HBV) but not in subjects with occult HBV infection. Aim: This study aimed to investigate the association of surface gene mutations with viral genotypes in occult HBV infection. Materials & Methods: Of 293 family contacts of 90 chronic HBV index patients, 110 consented for the study. Of 110 subjects, 97 were hepatitis B surface antigen (HBsAg) negative. HBV genotyping was done using direct DNA sequencing. The S‐gene was also sequenced in 13 chronic hepatitis B patients to serve as controls. Results: Twenty‐eight (28.8%) of the 97 subjects had occult HBV infection. Bidirectional sequencing of partial S‐gene was successful in 13 of them. Seven (53.8%) of the viral sequences are genotype A1, two (15.3%) each having genotypes D5&D2 and one each (7.6%) having D1&G genotypes. Seven (53.8%) of the 13 HBsAg positive patients, had genotype D&6 (46.1%) genotype A. A128V & T143M mutations were observed in 5 of 13 (38.4%) subjects and A128V & P127S in 2 of 13 (15.3%) patients ( P = 0.385). A128V mutation was seen in two (15.3%) subjects with D2 genotype, while T143M mutation was seen in three (23.07%) subjects with A1genotype. At aa125, three (23.07%) subjects with D5 genotype had methionine instead of threonine. There were wild type sequences in five (38.4%) subjects, one each of D1, G genotypes (20%) and four A1 (80%) genotypes. None of the subjects had G145R mutation. Conclusions: Occult HBV infection may be common in household contacts of chronic HBV infected patients. Equal prevalence of A&D sub‐genotypes was present in occult HBV subjects and in chronic HBV patients. Mutations of the S‐gene are genotype specific in both occult as well as chronic HBV infection.