Mutations in the S gene region of hepatitisB virus in high-risk patients with occult HBV infection
Abstract number: P1155
Ramezani A., Mohraz M., Hamkar R., Aghakhani A., Soufian S., Eslamifar A., Banifazl M.
Objective: Occult hepatitis B virus (HBV) infection is characterized by presence of HBV infection with undetectable hepatitis B surface antigen (HBsAg). Surface gene mutants (S mutants) have been reported in a variety of patient groups, with variable rates of occurrence. Due to the apparent increase in prevalence of S mutants and limited data regarding these mutations in patients with occult HBV infections; we aimed to determine the surface gene mutations of HBV among high risk patients with occult HBV infection.
Patients and Methods: In this study, 395 patients including 289 patients on chronic hemodialysis (HD) and 106 HIV infected subjects were enrolled. The presence of HBV-DNA was determined in plasma samples of patients with isolated anti-HBc (HBsAg negative, anti-HBs negative and anti-HBc positive) by real-time PCR. In HBV-DNA positive patients, surface gene region was amplified by nested PCR and surface gene mutations were analyzed after direct sequencing.
Results: HBV-DNA was detectable in 12 out of 40 patients (30%, 95% CI, 15.8%-44.2%) who had isolated anti-HBc. Of these 12 patients, 9 of them were HD patients and 3 of them were HIV infected subjects. Plasma HBV-DNA load was less than 50 IU/ml in all of these patients. In 8 patients (5 HD and 3 HIV infected patients) the amount of DNA was enough for analysis. In these patients, genotype and surface gene mutations were analyzed after direct sequencing. Phylogenetic analysis revealed that all of the HBV isolates were clustered in the Genotype D. Insertion of a T residue at position 60 and a G residue at position 89 were detected in 2 isolates. Premature stop codons were created in 2 other isolates via replacing of T by A at position 44 and G by T at position 28. The TTA to TAA stop mutation led to a premature stop codon at position Leu15 and the GGA to TGA led to a premature stop codon at position Gly10 in the S gene. Serine to asparagine substitution at residue 207 (S207N), due to a G to A transition at nucleotide position 620 was found in the other 4 sequences.
Conclusion: HBV genotype D was the only detectable genotype in Iranian patients with occult HBV infection. No "a" determinant mutations were detected in our isolates. This study suggested that the "a" region mutations did not play a major role in HBsAg detection and other mutations may be responsible for the existence of occult HBV infection and failure to detect HBsAg by routine laboratory tests.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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