Dynamic Analysis of HBV Infection Model with Simulations for Anti-HBV Infection Therapy

2011 ◽  
Author(s):  
Yu Zheng ◽  
Lequan Min ◽  
Xiao Chen ◽  
Yongan Ye
Keyword(s):  
Dynamic Analysis ◽  
Hbv Infection ◽  
Infection Model

scholarly journals Cross-Protection of Hepatitis B Vaccination among Different Genotypes

Vaccines ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 456
Author(s):  
Takako Inoue ◽  
Yasuhito Tanaka
Keyword(s):  
Hepatitis B ◽  
Cross Protection ◽  
Hbv Infection ◽  
Immune Memory ◽  
Hepatitis B Vaccination ◽  
Infection Model ◽  
Hbv Genotype ◽  
Hb Vaccine ◽  
Genotype A

Hepatitis B (HB) vaccination is the most effective method for preventing HB virus (HBV) infection. Universal HB vaccination containing recombinant HB surface antigens (HBsAg) is recommended. Our data revealed that human monoclonal HB surface antibody (anti-HBs) from individuals inoculated with genotype C-based HB vaccine induced cross-protection against HBV genotype A infection. An in vitro infection model demonstrated anti-HBs-positive sera from individuals inoculated with genotype A- or C-based HB vaccine harbored polyclonal anti-HBs that could bind to non-vaccinated genotype HBV. However, because there were low titers of anti-HBs specific for HBsAg of non-vaccinated genotype, high anti-HBs titers would be required to prevent non-vaccinated genotype HBV infection. Clinically, the 2015 Centers for Disease Control and Prevention guidelines state that periodic monitoring of anti-HBs levels after routine HB vaccination is not needed and that booster doses of HB vaccine are not recommended. However, the American Red Cross suggests that HB-vaccine-induced immune memory might be limited; although HB vaccination can prevent clinical liver injury (hepatitis), subclinical HBV infections of non-vaccinated genotypes resulting in detectable HB core antibody could not be completely prevented. Therefore, monitoring anti-HBs levels after routine vaccination might be necessary for certain subjects in high-risk groups.

Dynamics of a diffusion-driven HBV infection model with capsids and time delay

2017 ◽  
Vol 10 (05) ◽  
pp. 1750062 ◽  
Author(s):  
Kalyan Manna
Keyword(s):  
Steady State ◽  
Time Delay ◽  
Dynamical Behavior ◽  
Hbv Infection ◽  
Infection Model ◽  
Direct Lyapunov Method ◽  
Asymptotically Stable ◽  
Globally Asymptotically Stable ◽  
Discrete Time Delay ◽  
Number Formula

In this paper, a diffusive hepatitis B virus (HBV) infection model with a discrete time delay is presented and analyzed, where the spatial mobility of both intracellular capsid covered HBV DNA and HBV and the intracellular delay in the reproduction of infected hepatocytes are taken into account. We define the basic reproduction number [Formula: see text] that determines the dynamical behavior of the model. The local and global stability of the spatially homogeneous steady states are analyzed by using the linearization technique and the direct Lyapunov method, respectively. It is shown that the susceptible uninfected steady state is globally asymptotically stable whenever [Formula: see text] and is unstable whenever [Formula: see text]. Also, the infected steady state is globally asymptotically stable when [Formula: see text]. Finally, numerical simulations are carried out to illustrate the results obtained.

GLOBAL ANALYSIS OF A VIRAL INFECTION MODEL WITH APPLICATION TO HBV INFECTION

2010 ◽  
Vol 18 (02) ◽  
pp. 325-337 ◽  
Author(s):  
YU JI ◽  
LEQUAN MIN ◽  
YONGAN YE
Keyword(s):  
Viral Infection ◽  
Basic Reproduction Number ◽  
Reproduction Number ◽  
Global Analysis ◽  
Hiv Infections ◽  
Hbv Infection ◽  
Infection Model ◽  
Globally Asymptotically Stable ◽  
Reproduction Numbers ◽  
The Basic Reproduction Number

The basic models of within-host viral infection, proposed by Nowak and May2 and Perelson and Nelson,5 have been widely used in the studies of HBV and HIV infections. The basic reproduction numbers of the two models are proportional to the number of total cells of the host's organ prior to the infection. In this paper, we formulate an amended Perelson and Nelson's model with standard incidence. The basic reproduction number of the amended model is independent of total cells of the host's organ. If the basic reproduction number R0 < 1, then the infection-free equilibrium is globally asymptotically stable and the virus is cleared; if R0 > 1, then the virus persists in the host, and solutions approach either an endemic equilibrium or a periodic orbit. Numerical simulations of this model agree well with the clinical HBV infection data. This can provide a possible interpretation for the viral oscillation behaviors, which were observed in chronic HBV infection patients.

scholarly journals A generalized distributed delay model for HBV infection with two modes of transmission and adaptive immunity: A mathematical study

2021 ◽  
Author(s):  
Kalyan Manna ◽  
khalid hattaf
Keyword(s):  
Adaptive Immunity ◽  
Distributed Delay ◽  
Hbv Infection ◽  
Infection Model ◽  
Delay Model ◽  
Cell Infection ◽  
Modes Of Transmission ◽  
Proposed Model ◽  
Infection Models ◽  
B Virus

In this paper, we formulate a generalized hepatitis B virus (HBV) infection model with two modes of infection transmission and adaptive immunity, and investigate its dynamical properties. Both the virus-to-cell and cell-to-cell infection transmissions are modeled by general functions which satisfy some biologically motivated assumptions. Furthermore, the model incorporates three distributed time delays for the production of active infected hepatocytes, mature capsids and virions. The well-posedness of the proposed model is established by showing the non-negativity and boundedness of solu- tions. Five equilibria of the model are identified in terms of five threshold parameters R0, R1, R2, R3 and R4. Further, the global stability analysis of each equilibrium under certain conditions is carried out by employing suitable Lyapunov function and LaSalle’s invariance principle. Finally, we present an example with numerical simulations to il- lustrate the applicability of our study. Nonetheless, the results obtained in this study are valid for a wide class of HBV infection models.

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