prevalence of hepatitis B virus surface antigen [HBsAg] variations and correlation with the clinical and serologic pictures in chronic carriers from Khorasan Province, North-East of Iran

This study was designed to determine the correlation of hepatitis B virus surface Ag [HBsAg] variations with the clinical/serological pictures among chronic HBsAg positive patients. The surface gene [S-gene] was amplified and directly sequenced in twenty-five patients. Eight samples [group I] contained at least one mutation at the amino acid level. Five showed alanine aminotransferase [ALT] levels above the normal range of which only one sample was anti-HBe positive. Group II [17 samples] did not contain any mutation, 4 were anti-HBe positive and 9 had increased ALT levels. In both groups, from a total of 18 mutations, 5 [27.5%] and 13 [72.5%] occurred in anti-HBe and HBeAg positive groups respectively. The small number of amino acid mutations might belong to either the initial phase of chronicity in our patients; or that even in anti-HBe positive phase in Iranian genotype D-infected patients, a somehow tolerant pattern due to the host genetic factors may be responsible

Hepatitis B virus surface antigen variants clustered within immune epitopes in chronic hepatitis B carriers from hormozgan province, south of Iran

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. 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. 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 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. 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 B virus infection