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Conference Paper: Sequence Variations of Full-length Hepatitis B Virus Genomes in Chinese Patients with HBsAg-negative Hepatitis B Infection

TitleSequence Variations of Full-length Hepatitis B Virus Genomes in Chinese Patients with HBsAg-negative Hepatitis B Infection
Authors
Issue Date2015
PublisherSpandidos Publications.
Citation
Oral presentation at the 20th World Congress on Advances in Oncology and 18th International Symposium on Molecular Medicine, v. 36, Supplement 1 , p. S21 How to Cite?
AbstractThe underlying mechanism of HBsAg-negative hepatitis B virus (HBV) infection is notoriously difficult to elucidate because of the extremely low DNA levels which define the condition. We used a highly efficient amplification method to overcome this obstacle and achieved our aim which was to identify specific mutations or sequence variations associated with this entity. In this study, a total of 185 sera and 60 liver biopsies from HBsAg-negative, HBV DNA-positive subjects or known chronic hepatitis B (CHB) subjects with HBsAg seroclearance were amplified by rolling circle amplification followed by full-length HBV genome sequencing. Eleven HBsAg-positive CHB subjects were included as controls. The effects of pivotal mutations identified on regulatory regions on promoter activities were analyzed. A total of 22 and 11 full-length HBV genomes were amplified from HBsAg-negative and control subjects respectively. HBV genotype C was the dominant strain. A higher mutation frequency was observed in HBsAg-negative subjects than controls, irrespective of genotype. The nucleotide diversity over the entire HBV genome was significantly higher in HBsAg-negative subjects compared with controls (p = 0.008) and compared with 49 reference sequences from CHB patients (p = 0.025). In addition, HBsAg-negative subjects had significantly higher amino acid substitutions in the four viral genes than controls (all p < 0.001). Many mutations were uniquely found in HBsAg-negative subjects, including deletions in promoter regions (13.6%), abolishment of pre-S2/S start codon (18.2%), disruption of pre-S2/S mRNA splicing site (4.5%), nucleotide duplications (9.1%), and missense mutations in “α” determinant region, contributing to defects in HBsAg production. Taken together, these data suggest an accumulation of multiple mutations constraining viral transcriptional activities contribute to HBsAg-negativity in HBV infection. This study was supported by General Research Fund (HKU 782809)
Persistent Identifierhttp://hdl.handle.net/10722/229854

 

DC FieldValueLanguage
dc.contributor.authorHuang, FY-
dc.contributor.authorWong, DKH-
dc.contributor.authorSeto, WKW-
dc.contributor.authorZhang, AY-
dc.contributor.authorLee, CK-
dc.contributor.authorLin, CK-
dc.contributor.authorFung, JYY-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, RMF-
dc.date.accessioned2016-08-23T14:13:39Z-
dc.date.available2016-08-23T14:13:39Z-
dc.date.issued2015-
dc.identifier.citationOral presentation at the 20th World Congress on Advances in Oncology and 18th International Symposium on Molecular Medicine, v. 36, Supplement 1 , p. S21-
dc.identifier.urihttp://hdl.handle.net/10722/229854-
dc.description.abstractThe underlying mechanism of HBsAg-negative hepatitis B virus (HBV) infection is notoriously difficult to elucidate because of the extremely low DNA levels which define the condition. We used a highly efficient amplification method to overcome this obstacle and achieved our aim which was to identify specific mutations or sequence variations associated with this entity. In this study, a total of 185 sera and 60 liver biopsies from HBsAg-negative, HBV DNA-positive subjects or known chronic hepatitis B (CHB) subjects with HBsAg seroclearance were amplified by rolling circle amplification followed by full-length HBV genome sequencing. Eleven HBsAg-positive CHB subjects were included as controls. The effects of pivotal mutations identified on regulatory regions on promoter activities were analyzed. A total of 22 and 11 full-length HBV genomes were amplified from HBsAg-negative and control subjects respectively. HBV genotype C was the dominant strain. A higher mutation frequency was observed in HBsAg-negative subjects than controls, irrespective of genotype. The nucleotide diversity over the entire HBV genome was significantly higher in HBsAg-negative subjects compared with controls (p = 0.008) and compared with 49 reference sequences from CHB patients (p = 0.025). In addition, HBsAg-negative subjects had significantly higher amino acid substitutions in the four viral genes than controls (all p < 0.001). Many mutations were uniquely found in HBsAg-negative subjects, including deletions in promoter regions (13.6%), abolishment of pre-S2/S start codon (18.2%), disruption of pre-S2/S mRNA splicing site (4.5%), nucleotide duplications (9.1%), and missense mutations in “α” determinant region, contributing to defects in HBsAg production. Taken together, these data suggest an accumulation of multiple mutations constraining viral transcriptional activities contribute to HBsAg-negativity in HBV infection. This study was supported by General Research Fund (HKU 782809)-
dc.languageeng-
dc.publisherSpandidos Publications. -
dc.relation.ispartofOral presentation at the 20th World Congress on Advances in Oncology and 18th International Symposium on Molecular Medicine-
dc.titleSequence Variations of Full-length Hepatitis B Virus Genomes in Chinese Patients with HBsAg-negative Hepatitis B Infection -
dc.typeConference_Paper-
dc.identifier.emailHuang, FY: fungyu@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.emailFung, JYY: jfung@hkucc.hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityFung, JYY=rp00518-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, RMF=rp00479-
dc.identifier.hkuros262410-
dc.identifier.volume36, Supplement 1-
dc.identifier.spageS21-
dc.identifier.epageS21-
dc.publisher.placeLondon-

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