Viral Dynamics in hepatits B virus infection

Department of Zoology, University of Oxford, United Kingdom
Proceedings of the National Academy of Sciences (Impact Factor: 9.67). 05/1996; 93(9):4398-402. DOI: 10.1073/pnas.93.9.4398
Source: PubMed


Treatment of chronic hepatitis B virus (HBV) infections with the reverse transcriptase inhibitor lamivudine leads to a rapid decline in plasma viremia and provides estimates for crucial kinetic constants of HBV replication. We find that in persistently infected patients, HBV particles are cleared from the plasma with a half-life of approximately 1.0 day, which implies a 50% daily turnover of the free virus population. Total viral release into the periphery is approximately 10(11) virus particles per day. Although we have no direct measurement of the infected cell mass, we can estimate the turnover rate of these cells in two ways: (i) by comparing the rate of viral production before and after therapy or (ii) from the decline of hepatitis B antigen during treatment. These two independent methods give equivalent results: we find a wide distribution of half-lives for virus-producing cells, ranging from 10 to 100 days in different patients, which may reflect differences in rates of lysis of infected cells by immune responses. Our analysis provides a quantitative understanding of HBV replication dynamics in vivo and has implications for the optimal timing of drug treatment and immunotherapy in chronic HBV infection. This study also represents a comparison for recent findings on the dynamics of human immunodeficiency virus (HIV) infection. The total daily production of plasma virus is, on average, higher in chronic HBV carriers than in HIV-infected patients, but the half-life of virus-producing cells is much shorter in HIV. Most strikingly, there is no indication of drug resistance in HBV-infected patients treated for up to 24 weeks.

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    • "This sever disease can be transmitted easily through contact with infected body fluids[5]and it is, for example, 100 times more infectious than HIV (human immunodeficiency virus)[1,10]. In the last two decades, many mathematical models have been developed to describe and understand the dynamics of HBV infection[7,8,11]. Recently, some works have improved the previous models by replacing the constant infusion of healthy hepatocytes with a logistic growth function[2,3,6,9], this change enriches the dynamics of the HBV pathogenesis model. "

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    • "The basic model of HIV-1 infection involved evolution of three populations: uninfected cells, productively infected cells, and free viral particles, is governed by three-dimensional model of nonlinear ordinary differential equations (ODEs), see e.g., [24] [25] [27] [28] [29]. Recently, Rong et al., [30] improved the basic model of HIV-1 infection to four-dimensional ODE model, where an eclipse stage for the infected cells is included and a portion of these cells is reverted to the uninfected class. "
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    • "Mathematical models have been developed to explore mechanisms and dynamical behaviours of the inhost viral infection process. A basic virus dynamics model consists of the following simple three dimensional system (see [1] [2]): "
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