scholarly journals Mathematical Analysis and Treatment for a Delayed Hepatitis B Viral Infection Model with the Adaptive Immune Response and DNA-Containing Capsids

2018 ◽  
Vol 7 (4) ◽  
pp. 35 ◽  
Author(s):  
Jaouad Danane ◽  
Karam Allali
Keyword(s):  
Hepatitis B ◽  
Cytotoxic T Lymphocyte ◽  
Minimum Principle ◽  
Adaptive Immune Response ◽  
Finite Difference Approximation ◽  
Difference Approximation ◽  
Infection Model ◽  
Control Pair ◽  
B Virus ◽  
Hepatitis B Viral Infection

We model the transmission of the hepatitis B virus (HBV) by six differential equations that represent the reactions between HBV with DNA-containing capsids, the hepatocytes, the antibodies and the cytotoxic T-lymphocyte (CTL) cells. The intracellular delay and treatment are integrated into the model. The existence of the optimal control pair is supported and the characterization of this pair is given by the Pontryagin’s minimum principle. Note that one of them describes the effectiveness of medical treatment in restraining viral production, while the second stands for the success of drug treatment in blocking new infections. Using the finite difference approximation, the optimality system is derived and solved numerically. Finally, the numerical simulations are illustrated in order to determine the role of optimal treatment in preventing viral replication.

scholarly journals Discrete virus infection model of hepatitis B virus

2015 ◽  
Vol 26 (s1) ◽  
pp. S2187-S2195 ◽  
Author(s):  
Pengfei Zhang ◽  
Lequan Min ◽  
Jianwei Pian
Keyword(s):  
Hepatitis B Virus ◽  
Virus Infection ◽  
Hepatitis B ◽  
Infection Model ◽  
B Virus ◽  
Virus Infection Model

scholarly journals Efficient Generation of a Hepatitis B Virus Cytotoxic T Lymphocyte Epitope Requires the Structural Features of Immunoproteasomes

2000 ◽  
Vol 191 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Alice J.A.M. Sijts ◽  
Thomas Ruppert ◽  
Barbara Rehermann ◽  
Marion Schmidt ◽  
Ulrich Koszinowski ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Structural Features ◽  
Core Antigen ◽  
Ctl Epitope ◽  
Cleavage Specificity ◽  
B Virus ◽  
Ifn Γ

Interferon (IFN)-γ–induced cells express the proteasome subunits low molecular weight protein (LMP)2, LMP7, and MECL-1 (multicatalytic endopeptidase complex–like 1), leading to the formation of immunoproteasomes. Although these subunits are thought to optimize MHC class I antigen processing, the extent of their role and the mechanistic aspects involved remain unclear. Herein, we study the proteolytic generation of an human histocompatibility leukocyte antigen (HLA)-Aw68–restricted hepatitis B virus core antigen (HBcAg) cytotoxic T lymphocyte (CTL) epitope that is recognized by peripheral blood lymphocytes from patients with acute self-limited but not chronic hepatitis B virus (HBV). Immunological data suggest that IFN-γ–induced rather than uninduced HeLa cells process and present the HBV CTL epitope upon infection with HBcAg-expressing vaccinia viruses. Analyses of 20S proteasome digests of synthetic polypeptides covering the antigenic HBcAg peptide demonstrate that only immunoproteasomes efficiently perform the cleavages needed for the liberation of this HBV CTL epitope. Although the concerted presence of the three immunosubunits appears essential, we find that both catalytically active LMP7 and inactive LMP7 T1A support CTL epitope generation. We conclude that LMP7 influences the structural features of 20S proteasomes, thereby enhancing the activity of the LMP2 and MECL-1 catalytic sites, which provide cleavage specificity. Thus, LMP7 incorporation is of greater functional importance for the generation of an HBV CTL epitope than cleavage specificity.

Retrotransposon elements among initial sites of hepatitis B virus integration into human genome in the HepG2-NTCP cell infection model

2019 ◽  
Vol 235-236 ◽  
pp. 39-56 ◽  
Author(s):  
Ranjit Chauhan ◽  
Yoshimi Shimizu ◽  
Koichi Watashi ◽  
Takaji Wakita ◽  
Masayoshi Fukasawa ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Human Genome ◽  
Infection Model ◽  
Cell Infection ◽  
B Virus ◽  
Virus Integration

scholarly journals Binding of biotin to hepatitis B surface antigen: a possible pitfall in immunohistochemistry.

1989 ◽  
Vol 37 (4) ◽  
pp. 551-554 ◽  
Author(s):  
J J van den Oord ◽  
F Facchetti ◽  
C de Wolf-Peeters ◽  
V J Desmet
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Disulfide Bonds ◽  
Hepatitis B Surface Antigen ◽  
B Virus ◽  
Infected Liver ◽  
Hepatitis B Viral Infection ◽  
Positive Results

We report on the binding of biotin, and hence of biotinylated antibodies and lectins, to ground glass hepatocytes and liver cell membranes in chronic hepatitis B viral infection. This binding is of low affinity, and was proved to be directed at the hepatitis B surface antigen, presumably at its disulfide bonds. To avoid false-positive results, this affinity should be considered in the interpretation of immunohistochemical stainings of hepatitis B virus-infected liver tissue with biotinylated reagents.

Is antigenic variability a strategy adopted by hepatitis B virus to escape cytotoxic T-lymphocyte surveillance?

1996 ◽  
Vol 7 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Carlo Ferrari ◽  
Antonio Bertoletti ◽  
Franco Fiaccadori ◽  
Francis V. Chisari*
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Antigenic Variability ◽  
B Virus
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