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Occult hepatitis B virus infection: influence of S protein variants.

ABSTRACT: In occult hepatitis B viral infection (OBI), the persistence of hepatitis B virus (HBV) DNA is associated with a lack of hepatitis B surface antigen (HBsAg). To assess the possible role of HBsAg immune escape variants in OBI patients, variability in the HBV S gene was evaluated for OBI patients as well as chronic HBV infection patients from the same families.We selected 17 HBV DNA-positive/HBsAg-negative patients (OBI group) and 15 HBV DNA- and HBsAg-positive patients from OBI families (control group). The S gene was amplified and cloned, and at least 15 clones per patient were sequenced and analyzed.Although the incidence of stop codon mutations within the S region was higher in the OBI group (13.6 %) than in the control group (1.5 %, P < 0.001), this type of mutation, together with insertion and deletion mutations, was prevalent in only three OBI patients. In the major hydrophilic region (MHR), a median of 0.75 residues were altered in every 100 residues for the OBI patients, whereas 0.95 out of 100 residues were changed in the control group (P = 0.428). Furthermore, some variants that are generally considered immune escape variants, such as mutations at positions s145, s147, and s123, were only observed in less than 5 % of all the clones sequenced, in either OBI or control group.Our data suggest that HBsAg variants may not play a major role in OBI pathogenesis.

SUBMITTER: Zhang Z

PROVIDER: S-EPMC4717550 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

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Occult hepatitis B virus infection: influence of S protein variants.

Zhang Zhenhua Z Zhang Ling L Dai Yu Y Zhang Yafei Y Li Jun J Li Xu X

Virology journal 20160119

<h4>Background</h4>In occult hepatitis B viral infection (OBI), the persistence of hepatitis B virus (HBV) DNA is associated with a lack of hepatitis B surface antigen (HBsAg). To assess the possible role of HBsAg immune escape variants in OBI patients, variability in the HBV S gene was evaluated for OBI patients as well as chronic HBV infection patients from the same families.<h4>Methods</h4>We selected 17 HBV DNA-positive/HBsAg-negative patients (OBI group) and 15 HBV DNA- and HBsAg-positive p ...[more]

PMID: 26786229

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Project description:Background & objectivesNon-detection of hepatitis B virus (HBV) envelope protein (hepatitis B surface antigen, HBsAg) in a chronically HBV infected individual has been described as occult infection. One possible reason for this phenotype is alteration in large (L-HBsAg) to small (S-HBsAg) envelope protein ratio associated with reduced or non secretion of HBsAg. This results in quantitative levels of serum HBsAg below the detection limit of enzyme immunoassays. Genotype D of HBV has a characteristic 33 nucleotide (nt) deletion upstream of the pre-S2/S promoter. This deletion may reduce HBsAg secretion in occult infection patients infected with genotype D HBV. Additional deletions in the pre-S2/S promoter may further aggravate reduced HBsAg secretion in patients infected with genotype D HBV. Thus, the aim of the present study was to determine the role of genotype D specific 33nt deletion and additional pre-S2/S promoter deletions in causing reduced or no secretion of HBsAg, in occult infection. Since these deletions overlap virus polymerase, their effect on virus replication was also investigated.MethodsWe examined the in vitro expression of HBsAg, ratio of cure and 'e' antigen (HBcAg/HBeAg), their secretion and virus replication, using overlength 1.3 mer/1.86 mer genotype A replicons, and genotype D replicons with and without additional pre-S2/S promoter deletions from cases of occult infection.ResultsGenotype D replicon showed a decrease in HBsAg secretion compared to the wild-type genotype A. Genotype D replicons carrying additional pre-S2/S promoter deletions, showed further reduction in HBsAg secretion, demonstrated presence of intracellular HBcAg/HBeAg, virus replication intermediates and 'e' antigen secretion.Interpretation & conclusionsThe characteristic 33 nt deletion of genotype D HBV reduces HBsAg secretion. Additional pre-S2/S promoter deletions may further diminish HBsAg secretion, leading to occult infection. Pre-S2/S promoter deletions do not affect HBV replication.

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Occult hepatitis B virus infection: influence of S protein variants.

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Occult hepatitis B virus infection: influence of S protein variants.

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