A conservation law for virus infection kinetics in vitro

Kakizoe, Yusuke; Morita, Satoru; Nakaoka, Shinji; Takeuchi, Yasuhiro; Sato, Kei; Miura, Tomoyuki; Beauchemin, C.; Iwami, Shingo

doi:10.1016/j.jtbi.2015.03.034

Cited by 13 publications

(13 citation statements)

References 21 publications

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“…No explicit immune response is considered in this model since accurate information about its role in viral infections is still lacking [44]. Finally, this model assumes exponential distributions for eclipse and infectious transition times, which is known to be biologically unrealistic [26,53], but simplifies the computation and should not affect the qualitative predictions of the model. Our model is similar to those of [27,54] except that they include non-exponential distributions as well as non infectious virus particles in their models.…”

Section: Methods and Model Mathematical Modelmentioning

confidence: 99%

Coinfections of the Respiratory Tract: Viral Competition for Resources

2016

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Studies have shown that simultaneous infection of the respiratory tract with at least two viruses is common in hospitalized patients, although it is not clear whether these infections are more or less severe than single virus infections. We use a mathematical model to study the dynamics of viral coinfection of the respiratory tract in an effort to understand the kinetics of these infections. Specifically, we use our model to investigate coinfections of influenza, respiratory syncytial virus, rhinovirus, parainfluenza virus, and human metapneumovirus. Our study shows that during coinfections, one virus can block another simply by being the first to infect the available host cells; there is no need for viral interference through immune response interactions. We use the model to calculate the duration of detectable coinfection and examine how it varies as initial viral dose and time of infection are varied. We find that rhinovirus, the fastest-growing virus, reduces replication of the remaining viruses during a coinfection, while parainfluenza virus, the slowest-growing virus is suppressed in the presence of other viruses.

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Section: Methods and Model Mathematical Modelmentioning

confidence: 99%

Coinfections of the Respiratory Tract: Viral Competition for Resources

2016

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“…[45][46][47] Finally, exponential distributions for eclipse and infectious transition times are considered to simplify the computation even though it is known to be biologically unrealistic (a cell is not able to produce virus as soon as it is infected). 48,49…”

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confidence: 99%

The impact of cell regeneration on the dynamics of viral coinfection

Pinky

Dobrovolny

2017

Chaos: An Interdisciplinary Journal of Nonlinear Science

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Many mathematical models of respiratory viral infections do not include regeneration of cells within the respiratory tract, arguing that the infection is resolved before there is significant cellular regeneration. However, recent studies have found that ∼40% of patients hospitalized with influenza-like illness are infected with at least two different viruses, which could potentially lead to longer-lasting infections. In these longer infections, cell regeneration might affect the infection dynamics, in particular, allowing for the possibility of chronic coinfections. Several mathematical models have been used to describe cell regeneration in infection models, though the effect of model choice on the predicted time course of viral coinfections is not clear. We investigate four mathematical models incorporating different mechanisms of cell regeneration during respiratory viral coinfection to determine the effect of cell regeneration on infection dynamics. We perform linear stability analysis for each of the models and find the steady states analytically. The analysis suggests that chronic illness is possible but only with one viral species; chronic coexistence of two different viral species is not possible with the regeneration models considered here.

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“…Note that c, g, and δ include the removal of virus, and of the uninfected and infected cells, due to the experimental samplings. In our earlier works (Iwami et al, 2012a(Iwami et al, , 2012bFukuhara et al, 2013;Kakizoe et al, 2015), we have shown that the approximating punctual removal as a continuous exponential decay has minimal impact on the model parameters and provides an appropriate fit to the experimental data. In addition, we introduce the parameter ω, describing the infection rate via cell-to-cell contacts (Sourisseau et al, 2007;Sattentau, 2008;Sigal et al, 2011).…”

Section: Resultsmentioning

confidence: 94%

Decision letter: Cell-to-cell infection by HIV contributes over half of virus infection

2015

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Cell-to-cell viral infection, in which viruses spread through contact of infected cell with surrounding uninfected cells, has been considered as a critical mode of virus infection. However, since it is technically difficult to experimentally discriminate the two modes of viral infection, namely cell-free infection and cell-to-cell infection, the quantitative information that underlies cell-to-cell infection has yet to be elucidated, and its impact on virus spread remains unclear. To address this fundamental question in virology, we quantitatively analyzed the dynamics of cell-to-cell and cell-free human immunodeficiency virus type 1 (HIV-1) infections through experimental-mathematical investigation. Our analyses demonstrated that the cell-to-cell infection mode accounts for approximately 60% of viral infection, and this infection mode shortens the generation time of viruses by 0.9 times and increases the viral fitness by 3.9 times. Our results suggest that even a complete block of the cell-free infection would provide only a limited impact on HIV-1 spread.

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A conservation law for virus infection kinetics in vitro

Cited by 13 publications

References 21 publications

Coinfections of the Respiratory Tract: Viral Competition for Resources

Coinfections of the Respiratory Tract: Viral Competition for Resources

The impact of cell regeneration on the dynamics of viral coinfection

Decision letter: Cell-to-cell infection by HIV contributes over half of virus infection

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