scholarly journals T-Cell Response to Hepatitis B Core Antigen: Identification of Prior Exposure to and Confirmatory Testing for Screening for Anti-HBc

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Patricia Araujo ◽  
Roger Y. Dodd ◽  
Flavia Latinni ◽  
Renata Souza ◽  
Ricardo Diaz ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Cell Response ◽  
T Cell Response ◽  
Prior Exposure ◽  
Core Antigen ◽  
Confirmatory Testing ◽  
Hepatitis B Core Antigen

Role for CD4 positive T cell response in the pathogenesis of hepatitis B

1997 ◽  
Vol 26 (5) ◽  
pp. 1157
Author(s):  
Gerd R. Pape ◽  
Maria Christina Jung
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Cell Response ◽  
T Cell Response

scholarly journals The Size of the Viral Inoculum Contributes to the Outcome of Hepatitis B Virus Infection

2009 ◽  
Vol 83 (19) ◽  
pp. 9652-9662 ◽  
Author(s):  
Shinichi Asabe ◽  
Stefan F. Wieland ◽  
Pratip K. Chattopadhyay ◽  
Mario Roederer ◽  
Ronald E. Engle ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
T Cell ◽  
Hepatitis B ◽  
Cell Response ◽  
T Cell Response ◽  
Cd4 T Cell ◽  
Viral Spread ◽  
B Virus ◽  
T Cell Priming ◽  
Kinetics Of

ABSTRACT The impact of virus dose on the outcome of infection is poorly understood. In this study we show that, for hepatitis B virus (HBV), the size of the inoculum contributes to the kinetics of viral spread and immunological priming, which then determine the outcome of infection. Adult chimpanzees were infected with a serially diluted monoclonal HBV inoculum. Unexpectedly, despite vastly different viral kinetics, both high-dose inocula (1010 genome equivalents [GE] per animal) and low-dose inocula (10° GE per animal) primed the CD4 T-cell response after logarithmic spread was detectable, allowing infection of 100% of hepatocytes and requiring prolonged immunopathology before clearance occurred. In contrast, intermediate (107 and 104 GE) inocula primed the T-cell response before detectable logarithmic spread and were abruptly terminated with minimal immunopathology before 0.1% of hepatocytes were infected. Surprisingly, a dosage of 101 GE primed the T-cell response after all hepatocytes were infected and caused either prolonged or persistent infection with severe immunopathology. Finally, CD4 T-cell depletion before inoculation of a normally rapidly controlled inoculum precluded T-cell priming and caused persistent infection with minimal immunopathology. These results suggest that the relationship between the kinetics of viral spread and CD4 T-cell priming determines the outcome of HBV infection.

T-Cell Response to Hepatitis B and C Virus: Lessons from the Chimpanzee Model

2005 ◽  
pp. 66-80
Author(s):  
R. Thimme ◽  
J. Bukh ◽  
H.C. Spangenberg ◽  
S.F. Wieland ◽  
H.E. Blum ◽  
...  
Keyword(s):  
T Cell ◽  
Hepatitis B ◽  
Cell Response ◽  
T Cell Response

scholarly journals Cytotoxic T-Lymphocyte Antigen 4 Gene and Recovery from Hepatitis B Virus Infection

2004 ◽  
Vol 78 (20) ◽  
pp. 11258-11262 ◽  
Author(s):  
Chloe L. Thio ◽  
Timothy L. Mosbruger ◽  
Richard A. Kaslow ◽  
Christopher L. Karp ◽  
Steffanie A. Strathdee ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
T Cell ◽  
Hepatitis B ◽  
T Lymphocyte ◽  
Cell Response ◽  
Cytotoxic T Lymphocyte ◽  
Viral Persistence ◽  
T Cell Response ◽  
Hbv Infection ◽  
B Virus

ABSTRACT Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is an inhibitory T-cell receptor expressed by activated and regulatory T cells. We hypothesized that single-nucleotide polymorphisms (SNPs) in the gene encoding CTLA-4 may affect the vigor of the T-cell response to hepatitis B virus (HBV) infection, thus influencing viral persistence. To test this hypothesis, we genotyped six CTLA4 SNPs, from which all frequent haplotypes can be determined, using a large, matched panel of subjects with known HBV outcomes. Haplotypes with these SNPs were constructed for each subject using PHASE software. The haplotype distribution differed between those with viral persistence and those with clearance. Two haplotypes were associated with clearance of HBV infection, which was most likely due to associations with the SNPs −1722C (odds ratio [OR] = 0.60, P = 0.06) and +49G (OR = 0.73, P = 0.02). The wild-type haplotype, which contains an SNP leading to a decreased T-cell response (+6230A), was associated with viral persistence (OR = 1.32, P = 0.04). These data suggest that CTLA4 influences recovery from HBV infection, which is consistent with the emerging role of T regulatory cells in the pathogenesis of disease.

Recombinant hepatitis B large surface antigen, successfully produced in Escherichia coli, stimulates T-cell response in mice

Vaccine ◽  
2006 ◽  
Vol 24 (20) ◽  
pp. 4409-4416 ◽  
Author(s):  
Li Shu ◽  
Neal Touzjian ◽  
Deng Nan ◽  
Nicholas Kushner ◽  
Amie J. Strong ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
T Cell ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Cell Response ◽  
T Cell Response ◽  
Recombinant Hepatitis

CD8+ T-Cell Responses in Hepatitis B and C: The (HLA-) A, B, and C of Hepatitis B and C

2016 ◽  
Vol 34 (4) ◽  
pp. 396-409 ◽  
Author(s):  
Katja Nitschke ◽  
Hendrik Luxenburger ◽  
Muthamia M. Kiraithe ◽  
Robert Thimme ◽  
Christoph Neumann-Haefelin
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hepatitis B ◽  
Cd8 T Cells ◽  
Cell Response ◽  
Acute Infection ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Hcv Infection ◽  
T Cell Epitopes

Approximately 500 million people are chronically infected with the hepatitis B virus (HBV) or hepatitis C virus (HCV) worldwide and are thus at high risk of progressive liver disease, leading to liver fibrosis, cirrhosis and ultimately hepatocellular cancer. Virus-specific CD8+ T-cells play a major role in viral clearance in >90% of adult patients who clear HBV and in approximately 30% of patients who clear HCV in acute infection. However, several mechanisms contribute to the failure of the adaptive CD8+ T-cell response in those patients who progress to chronic infection. These include viral mutations leading to escape from the CD8+ T-cell response as well as exhaustion and dysfunction of virus-specific CD8+ T-cells. Antiviral efficacy of the virus-specific CD8+ T-cell response also strongly depends on its restriction by specific human leukocyte antigens (HLA) class I alleles. Our review will summarize the role of HLA-A, B and C-restricted CD8+ T-cells in HBV and HCV infection. Due to the current lack of a comprehensive database of HBV- and HCV-specific CD8+ T-cell epitopes, we also provide a summary of the repertoire of currently well-described HBV- and HCV-specific CD8+ T-cell epitopes. A better understanding of the factors that contribute to the success or failure of virus-specific CD8+ T-cells may help to develop new therapeutic options for HBV eradication in patients with chronic HBV infection (therapeutic vaccination and/or immunomodulation) as well as a prophylactic vaccine against HCV infection.

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