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      Multi-scale problem in the model of RNA virus evolution

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          Abstract

          A mathematical or computational model in evolutionary biology should necessary combine several comparatively fast processes, which actually drive natural selection and evolution, with a very slow process of evolution. As a result, several very different time scales are simultaneously present in the model; this makes its analytical study an extremely difficult task. However, the significant difference of the time scales implies the existence of a possibility of the model order reduction through a process of time separation. In this paper we conduct the procedure of model order reduction for a reasonably simple model of RNA virus evolution reducing the original system of three integro-partial derivative equations to a single equation. Computations confirm that there is a good fit between the results for the original and reduced models.

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          Modeling plasma virus concentration during primary HIV infection.

          During primary HIV infection the viral load in plasma increases, reaches a peak, and then declines. Phillips has suggested that the decline is due to a limitation in the number of cells susceptible to HIV infection, while other authors have suggested that the decline in viremia is due to an immune response. Here we address this issue by developing models of primary HIV-1 infection, and by comparing predictions from these models with data from ten anti-retroviral, drug-naive, infected patients. Applying nonlinear least-squares estimation, we find that relatively small variations in parameters are capable of mimicking the highly diverse patterns found in patient viral load data. This approach yields an estimate of 2.5 days for the average lifespan of productively infected cells during primary infection, a value that is consistent with results obtained by drug perturbation experiments. We find that the data from all ten patients are consistent with a target-cell-limited model from the time of initial infection until shortly after the peak in viremia. However, the kinetics of the subsequent fall and recovery in virus concentration in some patients are not consistent with the predictions of the target-cell-limited model. We illustrate that two possible immune response mechanisms, cytotoxic T lymphocyte destruction of infected target cells and cytokine suppression of viral replication, could account for declines in viral load data not predicted by the original target-cell-limited model. We conclude that some additional process, perhaps mediated by CD8+ T cells, is important in at least some patients. Copyright 2000 Academic Press.
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            Global properties of basic virus dynamics models.

            Lyapunov functions for basic virus dynamics models are introduced, and global stability of the models are thereby established.
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              RNA Virus Evolution via a Fitness-Space Model

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                Author and article information

                Journal
                J Phys Conf Ser
                J Phys Conf Ser
                jpcs
                Journal of Physics. Conference Series
                IOP Publishing
                1742-6588
                1742-6596
                June 2016
                : 727
                : 1
                : 012007
                Affiliations
                [JPCS_727_1_0120071 ]Centre de Recerca Matemática , Campus de Bellaterra , Edifici C , 08193 Barcelona, Spain akorobeinikov@ 123456crm.cat
                [JPCS_727_1_0120072 ]Departament de Matemàtiques, Universitat Autònoma de Barcelona , Campus de Bellaterra , Edifici C , 08193 Barcelona, Spain aarchibasov@ 123456gmail.com
                [JPCS_727_1_0120073 ]Department of Applied Mathematics Samara State Aerospace University (SSAU), 34, Moskovskoye shosse, Samara 443086, Russia hsablem@ 123456gmail.com
                [JPCS_727_1_0120074 ]Department of Technical Cybernetics Samara State Aerospace University (SSAU), 34, Moskovskoye shosse, Samara 443086, Russia
                Article
                JPCS_727_1_012007 J7271007
                10.1088/1742-6596/727/1/012007
                7106948
                172f74d4-0aed-41ba-93b9-c70622a521dc
                Published under licence by IOP Publishing Ltd

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                Content from this work may be used under the terms of the Creative Commons Attribution 3.0 licence. Any further distribution of this work must maintain attribution to the author(s) and the title of the work, journal citation and DOI.

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                Pages: 9
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