The Impact of Hepatitis B Virus Precore/Core Gene Carboxyl Terminal Mutations on Viral Biosynthesis and the Host Immune Response

Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis Be antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV–infected patients. Methods. We analyzed the HBV precore/core gene sequences...

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Published inThe Journal of infectious diseases Vol. 209; no. 9; pp. 1374 - 1381
Main Authors Wu, Jia-Feng, Ni, Yen-Hsuan, Chen, Huey-Ling, Hsu, Hong-Yuan, Chang, Mei-Hwei
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.05.2014
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Abstract Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis Be antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV–infected patients. Methods. We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV–infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3⁺ CD8⁺ T lymphocytes of chronic HBV–infected subjects. Results. The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P=.01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3⁺ CD8⁺ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). Conclusions. The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
AbstractList Background.  We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV–infected patients. Methods.  We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV–infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3+CD8+ T lymphocytes of chronic HBV–infected subjects. Results.  The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3+CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). Conclusions.  The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV-infected patients.BACKGROUND We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV-infected patients. We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV-infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3+ CD8+ T lymphocytes of chronic HBV-infected subjects.METHODS We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV-infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3+ CD8+ T lymphocytes of chronic HBV-infected subjects. The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3+ CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03).RESULTS The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3+ CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.CONCLUSIONS The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis Be antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV–infected patients. Methods. We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV–infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3⁺ CD8⁺ T lymphocytes of chronic HBV–infected subjects. Results. The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P=.01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3⁺ CD8⁺ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). Conclusions. The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV-infected patients.  We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV-infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3+ CD8+ T lymphocytes of chronic HBV-infected subjects.  The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon-γ expression in CD3+ CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03).  The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human immune responses in chronic HBV&-; infected patients. Methods. We analyzed the HBV precore/core gene sequences by cloning method in 33 chronic HBV&-; infected patients during the inflammatory phase before spontaneous HBeAg seroconversion. The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and native agarose gel analysis in Huh7 cells, and the human immune responses were assessed by in vitro stimulation of CD3 super(+)CD8 super(+) T lymphocytes of chronic HBV-infected subjects. Results. The P135Q and G1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P = .01 and <.001, respectively). The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells. The P135Q mutant peptide induced less interferon- gamma expression in CD3 super(+)CD8 super(+) T lymphocytes in HBeAg-negative subjects compared to the wild-type peptide (P = .03). Conclusions. The HBV P135Q mutant emergence during the inflammatory phase was associated with HBeAg seroconversion. It was associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses following HBeAg seroconversion.
Author Chen, Huey-Ling
Hsu, Hong-Yuan
Chang, Mei-Hwei
Wu, Jia-Feng
Ni, Yen-Hsuan
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Cites_doi 10.1016/j.virol.2009.03.002
10.1203/01.PDR.0000242270.91973.ff
10.1128/JVI.00608-12
10.1128/JVI.78.24.13812-13818.2004
10.1203/01.PDR.0000136282.20470.87
10.1073/pnas.1834404100
10.1002/hep.21482
10.1016/j.ajpath.2012.03.036
10.1099/0022-1317-76-4-1041
10.1128/JVI.76.12.5985-5992.2002
10.1128/JVI.77.23.12875-12880.2003
10.1128/JVI.02348-08
10.1053/j.gastro.2007.06.011
10.1053/j.gastro.2004.09.048
10.1053/jhep.2000.8529
10.1016/S1097-2765(01)80009-5
10.1016/S0016-5085(00)70261-7
10.1016/S0168-8278(98)80337-1
10.1016/j.jcv.2004.10.002
10.1136/gut.52.1.122
10.1002/(SICI)1096-9071(200003)60:3<256::AID-JMV2>3.0.CO;2-H
10.1111/j.1365-2893.2005.00552.x
10.1016/S0140-6736(81)90585-7
10.1016/j.jhep.2004.06.031
10.1056/NEJMoa013215
10.1128/JVI.65.12.6817-6825.1991
10.1073/pnas.88.10.4186
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Copyright Copyright © 2014 Oxford University Press on behalf of the Infectious Diseases Society of America
The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com . 2013
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Issue 9
Keywords immune escape mutant
precore/core gene
hepatitis B e antigen seroconversion
hepatitis B virus
hepatitis B e antigen
Virus
Infection
Immune response
Gene
Hepadnaviridae
Orthohepadnavirus
Biosynthesis
Mutation
Hepatitis B virus
Language English
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References Tsai ( key 20170425161358_JIT638C13) 2009; 387
Ito ( key 20170425161358_JIT638C11) 2009; 83
Schlicht ( key 20170425161358_JIT638C22) 1991; 65
Ni ( key 20170425161358_JIT638C27) 2004; 127
Laine ( key 20170425161358_JIT638C21) 2003; 77
Liu ( key 20170425161358_JIT638C1) 2005; 12
Carlier ( key 20170425161358_JIT638C12) 1995; 76
Beasley ( key 20170425161358_JIT638C3) 1981; 2
Lin ( key 20170425161358_JIT638C18) 2012; 86
Locarnini ( key 20170425161358_JIT638C23) 2005; 32
Yeh ( key 20170425161358_JIT638C15) 2004; 41
Lim ( key 20170425161358_JIT638C8) 2007; 133
Wynne ( key 20170425161358_JIT638C9) 1999; 3
Belnap ( key 20170425161358_JIT638C5) 2003; 19
Ni ( key 20170425161358_JIT638C17) 2004; 56
Ni ( key 20170425161358_JIT638C7) 2003; 52
Brunetto ( key 20170425161358_JIT638C24) 1991; 88
Wu ( key 20170425161358_JIT638C19) 2006; 60
Ni ( key 20170425161358_JIT638C6) 2000; 32
Wu ( key 20170425161358_JIT638C4) 2012; 181
Messageot ( key 20170425161358_JIT638C10) 1998; 273
Chang ( key 20170425161358_JIT638C14) 1998; 28
Yang ( key 20170425161358_JIT638C2) 2002; 347
Baumeister ( key 20170425161358_JIT638C20) 2000; 60
Sugauchi ( key 20170425161358_JIT638C16) 2002; 76
Kao ( key 20170425161358_JIT638C28) 2000; 118
Kock ( key 20170425161358_JIT638C26) 2004; 78
Visvanathan ( key 20170425161358_JIT638C25) 2007; 45
References_xml – volume: 387
  start-page: 364
  year: 2009
  ident: key 20170425161358_JIT638C13
  article-title: Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations
  publication-title: Virology
  doi: 10.1016/j.virol.2009.03.002
– volume: 60
  start-page: 602
  year: 2006
  ident: key 20170425161358_JIT638C19
  article-title: Impaired T-lymphocyte proliferation function in biliary atresia with chronic cholestatic jaundice after Kasai operation
  publication-title: Pediatr Res
  doi: 10.1203/01.PDR.0000242270.91973.ff
– volume: 86
  start-page: 9266
  year: 2012
  ident: key 20170425161358_JIT638C18
  article-title: Hepatitis B virus nucleocapsid but not free core antigen controls viral clearance in mice
  publication-title: J Virol
  doi: 10.1128/JVI.00608-12
– volume: 78
  start-page: 13812
  year: 2004
  ident: key 20170425161358_JIT638C26
  article-title: Hepatitis B virus nucleocapsids formed by carboxy-terminally mutated core proteins contain spliced viral genomes but lack full-size DNA
  publication-title: J Virol
  doi: 10.1128/JVI.78.24.13812-13818.2004
– volume: 56
  start-page: 396
  year: 2004
  ident: key 20170425161358_JIT638C17
  article-title: Longitudinal study on mutation profiles of core promoter and precore regions of the hepatitis B virus genome in children
  publication-title: Pediatr Res
  doi: 10.1203/01.PDR.0000136282.20470.87
– volume: 19
  start-page: 10884
  year: 2003
  ident: key 20170425161358_JIT638C5
  article-title: Diversity of core antigen epitopes of hepatitis B virus
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.1834404100
– volume: 45
  start-page: 102
  year: 2007
  ident: key 20170425161358_JIT638C25
  article-title: Regulation of toll-like receptor-2 expression in chronic hepatitis B by the precore protein
  publication-title: Hepatology
  doi: 10.1002/hep.21482
– volume: 181
  start-page: 19
  year: 2012
  ident: key 20170425161358_JIT638C4
  article-title: Suppression of furin by interferon-γ and the impact on hepatitis B virus antigen biosynthesis in human hepatocytes
  publication-title: Am J Pathol
  doi: 10.1016/j.ajpath.2012.03.036
– volume: 76
  start-page: 1041
  year: 1995
  ident: key 20170425161358_JIT638C12
  article-title: Importance of the C terminus of the hepatitis B virus precore protein in secretion of HBe antigen
  publication-title: J General Virol
  doi: 10.1099/0022-1317-76-4-1041
– volume: 76
  start-page: 5985
  year: 2002
  ident: key 20170425161358_JIT638C16
  article-title: Hepatitis B virus of genotype B with or without recombination with genotype C over the precore region plus the core gene
  publication-title: J Virol
  doi: 10.1128/JVI.76.12.5985-5992.2002
– volume: 77
  start-page: 12875
  year: 2003
  ident: key 20170425161358_JIT638C21
  article-title: In vitro and in vivo interactions between the hepatitis B virus protein P22 and the cellular protein gC1qR
  publication-title: J Virol
  doi: 10.1128/JVI.77.23.12875-12880.2003
– volume: 83
  start-page: 3507
  year: 2009
  ident: key 20170425161358_JIT638C11
  article-title: Characterization of genotype-specific carboxyl-terminal cleavage sites of hepatitis B virus e antigen precursor and identification of furin as the cleavage enzyme
  publication-title: J Virol
  doi: 10.1128/JVI.02348-08
– volume: 133
  start-page: 951
  year: 2007
  ident: key 20170425161358_JIT638C8
  article-title: Viral quasi-species evolution during hepatitis Be antigen seroconversion
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2007.06.011
– volume: 127
  start-page: 1733
  year: 2004
  ident: key 20170425161358_JIT638C27
  article-title: Clinical relevance of hepatitis B virus genotype in children with chronic infection and hepatocellular carcinoma
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2004.09.048
– volume: 32
  start-page: 124
  year: 2000
  ident: key 20170425161358_JIT638C6
  article-title: Long-term follow-up study of core gene deletion mutants in children with chronic hepatitis B virus infection
  publication-title: Hepatology
  doi: 10.1053/jhep.2000.8529
– volume: 3
  start-page: 771
  year: 1999
  ident: key 20170425161358_JIT638C9
  article-title: The crystal structure of human hepatitis B virus capsid
  publication-title: Mol Cell
  doi: 10.1016/S1097-2765(01)80009-5
– volume: 118
  start-page: 554
  year: 2000
  ident: key 20170425161358_JIT638C28
  article-title: Hepatitis B genotypes correlate with clinical outcomes in patients with chronic hepatitis B
  publication-title: Gastroenterology
  doi: 10.1016/S0016-5085(00)70261-7
– volume: 28
  start-page: 915
  year: 1998
  ident: key 20170425161358_JIT638C14
  article-title: Precore stop codon mutant in chronic hepatitis B virus infection in children: its relation to hepatitis B e antigen seroconversion and maternal hepatitis B surface antigen
  publication-title: J Hepatol
  doi: 10.1016/S0168-8278(98)80337-1
– volume: 32
  start-page: 113
  year: 2005
  ident: key 20170425161358_JIT638C23
  article-title: Cellular response to conditional expression of the hepatitis B virus precore and core proteins in cultured hepatoma (Huh-7) cells
  publication-title: J Clin Virol
  doi: 10.1016/j.jcv.2004.10.002
– volume: 273
  start-page: 18594
  year: 1998
  ident: key 20170425161358_JIT638C10
  article-title: The C terminus of the hepatitis B virus e antigen precursor is required for a tunicamycin-sensitive step that promotes efficient secretion of the antigen
  publication-title: J Virol
– volume: 52
  start-page: 122
  year: 2003
  ident: key 20170425161358_JIT638C7
  article-title: Different hepatitis B virus core gene mutations in children with chronic infection and hepatocellular carcinoma
  publication-title: Gut
  doi: 10.1136/gut.52.1.122
– volume: 60
  start-page: 256
  year: 2000
  ident: key 20170425161358_JIT638C20
  article-title: Hepatitis B virus e antigen specific epitopes and limitations of commercial anti-HBe immunoassays
  publication-title: J Med Virol
  doi: 10.1002/(SICI)1096-9071(200003)60:3<256::AID-JMV2>3.0.CO;2-H
– volume: 12
  start-page: 146
  year: 2005
  ident: key 20170425161358_JIT638C1
  article-title: Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance?
  publication-title: J Viral Hepat
  doi: 10.1111/j.1365-2893.2005.00552.x
– volume: 2
  start-page: 1129
  year: 1981
  ident: key 20170425161358_JIT638C3
  article-title: Hepatocellular carcinoma and hepatitis B virus: a prospective study of 22,707 men in Taiwan
  publication-title: Lancet
  doi: 10.1016/S0140-6736(81)90585-7
– volume: 41
  start-page: 659
  year: 2004
  ident: key 20170425161358_JIT638C15
  article-title: Quantification and genotyping of hepatitis B virus in a single reaction by real-time PCR and melting curve analysis
  publication-title: J Hepatol
  doi: 10.1016/j.jhep.2004.06.031
– volume: 347
  start-page: 168
  year: 2002
  ident: key 20170425161358_JIT638C2
  article-title: Hepatitis B e antigen and the risk of hepatocellular carcinoma
  publication-title: N Engl J Med
  doi: 10.1056/NEJMoa013215
– volume: 65
  start-page: 6817
  year: 1991
  ident: key 20170425161358_JIT638C22
  article-title: The quaternary structure, antigenicity, and aggregational behavior of the secretory core protein of human hepatitis B virus are determined by its signal sequence
  publication-title: J Virol
  doi: 10.1128/JVI.65.12.6817-6825.1991
– volume: 88
  start-page: 4186
  year: 1991
  ident: key 20170425161358_JIT638C24
  article-title: Wild-type and e antigen-minus hepatitis B viruses and course of chronic hepatitis
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.88.10.4186
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Snippet Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis Be antigen (HBeAg) seroconversion,...
Background.  We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg)...
We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV...
Background. We aimed to elucidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e antigen (HBeAg)...
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StartPage 1374
SubjectTerms Adult
Amino acids
Biological and medical sciences
Capsid
Capsid Proteins - immunology
Cell Line
Female
Fundamental and applied biological sciences. Psychology
Gene expression
Genetic mutation
Genotypes
Hepatitis antigens
Hepatitis B - immunology
Hepatitis B - virology
Hepatitis B Antibodies - blood
Hepatitis B Antibodies - immunology
Hepatitis B Core Antigens - genetics
Hepatitis B Core Antigens - immunology
Hepatitis B e Antigens - immunology
Hepatitis B virus
Hepatitis B virus - genetics
Hepatitis B virus - immunology
Host-Pathogen Interactions - immunology
Humans
Infectious diseases
Interferon-gamma - immunology
Male
Medical sciences
Microbiology
Miscellaneous
Mutation
Polymerase chain reaction
T lymphocytes
Transfection
Virology
VIRUSES
Young Adult
Title The Impact of Hepatitis B Virus Precore/Core Gene Carboxyl Terminal Mutations on Viral Biosynthesis and the Host Immune Response
URI https://www.jstor.org/stable/43708478
https://www.ncbi.nlm.nih.gov/pubmed/24273041
https://www.proquest.com/docview/1515646152
https://www.proquest.com/docview/1618159810
Volume 209
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