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In this paper, we develop an in-host mathematical model of snakebite envenoming that includes tissue, red blood and platelet cells of humans as specific targets of different kinds of toxins in the snake venom. The model is use to study some harmful effects of cytotoxic and hemotoxic snake venom on their target cells under the influence of snake antivenom. The model has two equilibrium points, namely, trivial and venom free. It has been shown that both the equilibrium points are globally asymptotically stable and numerical simulations illustrate the global asymptotic stability of the venom free equilibrium point. Furthermore, simulations reveal the importance of administering antivenom to avert the possible damage from venom toxins on the target cells. It is also shown through simulation that administering the required dose of antivenom can lead to the elimination of venom toxins within one week. Therefore, we recommend the administration of an adequate dose of antivenom therapy as it helps in deactivating venom toxins faster and consequently enhances the recovery time. [ABSTRACT FROM AUTHOR]

Mathematical models describing SARS-CoV-2 dynamics and the corresponding immune responses in patients with COVID-19 can be critical to evaluate possible clinical outcomes of antiviral treatments. In this work, based on the concept of virus spreadability in the host, antiviral effectiveness thresholds are determined to establish whether or not a treatment will be able to clear the infection. In addition, the virus dynamic in the host – including the time-to-peak and the final monotonically decreasing behavior – is characterized as a function of the time to treatment initiation. Simulation results, based on nine patient data, show the potential clinical benefits of a treatment classification according to patient critical parameters. This study is aimed at paving the way for the different antivirals being developed to tackle SARS-CoV-2. • A full dynamic characterization of a target cell-limited model for COVID-19 is presented. • Formal threshold values for the antiviral effectiveness are given. • A study of both, effective and ineffective treatments is made. • Simulation results show the potential benefits of the antiviral effectiveness characterization. [ABSTRACT FROM AUTHOR]

Recent clinical studies have shown that HIV disease pathogenesis can depend strongly on many factors at the time of transmission, including the strength of the initial viral load and the local availability of CD4+ T-cells. In this article, a new within-host model of HIV infection that incorporates the homeostatic proliferation of T-cells is formulated and analyzed. Due to the effects of this biological process, the influence of initial conditions on the proliferation of HIV infection is further elucidated. The identifiability of parameters within the model is investigated and a local stability analysis, which displays additional complexity in comparison to previous models, is conducted. The current study extends previous theoretical and computational work on the early stages of the disease and leads to interesting nonlinear dynamics, including a parameter region featuring bistability of infectious and viral clearance equilibria and the appearance of a Hopf bifurcation within biologically relevant parameter regimes. [ABSTRACT FROM AUTHOR]

While many epidemiological models were proposed to understand and handle COVID-19 pandemic, too little has been invested to understand human viral replication and the potential use of novel antivirals to tackle the infection. In this work, using a control theoretical approach, validated mathematical models of SARS-CoV-2 in humans are characterized. A complete analysis of the main dynamic characteristic is developed based on the reproduction number. The equilibrium regions of the system are fully characterized, and the stability of such regions is formally established. Mathematical analysis highlights critical conditions to decrease monotonically SARS-CoV-2 in the host, as such conditions are relevant to tailor future antiviral treatments. Simulation results show the aforementioned system characterization. [ABSTRACT FROM AUTHOR]

In this paper, a general viral model with virus-driven proliferation of target cells is studied. Global stability results are established by employing the Lyapunov method and a geometric approach developed by Li and Muldowney. It is shown that under certain conditions, the model exhibits a global threshold dynamics, while if these conditions are not met, then backward bifurcation and bistability are possible. An example is presented to provide some insights on how the virus-driven proliferation of target cells inuences the virus dynamics and the drug therapy strategies. [ABSTRACT FROM AUTHOR]

To understand joint effects of logistic growth in target cells and intracellular delay on viral dynamics in vivo, we carry out two-parameter bifurcation analysis of an in-host model that describes infections of many viruses including HIV-I, HBV and HTLV-I. The bifurcation parameters are the mitosis rate r of the target cells and an intracellular delay τ in the incidence of viral infection. We describe the stability region of the chronic-infection equilibrium E* in the two-dimensional ( r, τ) parameter space, as well as the global Hopf bifurcation curves as each of τ and r varies. Our analysis shows that, while both τ and r can destabilize E* and cause Hopf bifurcations, they do behave differently. The intracellular delay τ can cause Hopf bifurcations only when r is positive and sufficiently large, while r can cause Hopf bifurcations even when τ = 0. Intracellular delay τ can cause stability switches in E* while r does not. [ABSTRACT FROM AUTHOR]