BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=curation_notes.txthttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018-biopax2.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018-biopax3.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=manifest.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018-octave.mhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018-matlab.mhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018.odehttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=curation_image.pnghttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018.cpshttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=FatehiChenar2018.sedmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000848?filename=metadata.rdfprimaryOK200Johannes MeyerManually curatedordinary differential equation modelL2V4https://www.ebi.ac.uk/biomodels/BIOMD000000084829574141falseBioModelsSBMLModelsFatehiChenar2018 Mathematical model of immune response to hepatitis B2018MODEL1911110001F Fatehi Chenar, Y N Kyrychko, K B BlyussF Fatehi Chenar29574141, A new detailed mathematical model for dynamics of immune response to hepatitis B is proposed, which takes into account contributions from innate and adaptive immune responses, as well as cytokines. Stability analysis of different steady states is performed to identify parameter regions where the model exhibits clearance of infection, maintenance of a chronic infection, or periodic oscillations. Effects of nucleoside analogues and interferon treatments are analysed, and the critical drug efficiency is determined.. null, 447. Department of Mathematics, University of Sussex, Brighton BN1 9QH, UK.johannes.p.meyer@gmail.comEMBL-EBIBIOMD0000000848A new detailed mathematical model for dynamics of immune response to hepatitis B is proposed, which takes into account contributions from innate and adaptive immune responses, as well as cytokines. Stability analysis of different steady states is performed to identify parameter regions where the model exhibits clearance of infection, maintenance of a chronic infection, or periodic oscillations. Effects of nucleoside analogues and interferon treatments are analysed, and the critical drug efficiency is determined.A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease. Productively infected cells were estimated to have, on average, a life-span of 2.2 days (half-life t 1/2 = 1.6 days), and plasma virions were estimated to have a mean life-span of 0.3 days (t 1/2 = 0.24 days). The estimated average total HIV-1 production was 10.3 x 10(9) virions per day, which is substantially greater than previous minimum estimates. The results also suggest that the minimum duration of the HIV-1 life cycle in vivo is 1.2 days on average, and that the average HIV-1 generation time--defined as the time from release of a virion until it infects another cell and causes the release of a new generation of viral particles--is 2.6 days. These findings on viral dynamics provide not only a kinetic picture of HIV-1 pathogenesis, but also theoretical principles to guide the development of treatment strategies.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.Viral dynamics in hepatitis B virus infection.HIV-1 dynamics in vivo: virion clearance rate, infected cell life-span, and viral generation time.Mathematical model of immune response to hepatitis B.Nowak M A MA, Bonhoeffer S S, Hill A M AM, Boehme R R, Thomas H C HC, McDade H HFatehi Chenar F F, Kyrychko Y N YN, Blyuss K B KBPerelson A S AS, Neumann A U AU, Markowitz M M, Leonard J M JM, Ho D D DDfalseFatehiChenar2018 - Mathematical model of immune response to hepatitis B This is a mathematical model describing the dynamics of the immune response to hepatitis B, which takes into account contributions form innate and adaptive immune responses, as well as cytokines. 2024-08-222024-09-022019-11-11BIOMD0000000848SBO:0000179PR:000025848PR:0000249902957414185991148633078C13041NCIT:C3097NCIT:C14215NCIT:C38014NCIT:C62795C75958C20493NCIT:C95533BIOMD0000000848MODEL1911110001GO:0006955GO:0008219GO:0046718GO:0001906GO:0032606GO:0032609GO:0001787GO:0032819GO:0045065GO:0046753GO:0048305CL:0000910CL:0000182CL:0000623BTO:0000152000146010.1109/ISB.2012.6314119