Publications by authors named "Vitaly Volpert"

The process of viral infection spreading in tissues was influenced by various factors, including virus replication within host cells, transportation, and the immune response. Reaction-diffusion systems provided a suitable framework for examining this process. In this work, we studied a nonlocal reaction-diffusion system of equations that modeled the distribution of viruses based on their genotypes and their interaction with the immune response.

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Unlabelled: In the present study, we investigated traveling waves induced by transcranial alternating current stimulation in the alpha frequency band of healthy subjects. Electroencephalographic data were recorded in 12 healthy subjects before, during, and after phase-shifted stimulation with a device combining both electroencephalographic and stimulation capacities. In addition, we analyzed the results of numerical simulations and compared them to the results of identical analysis on real EEG data.

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We introduce and study a new model for the progression of Alzheimer's disease (AD) incorporating the interactions of A -monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. To understand the complete interactions between these elements, we study a spatially homogeneous simplified model that allows us to determine the effect of key parameters such as degradation rates in the asymptotic behaviour of the system and the stability of equilibrium. We observe that inflammation appears to be a crucial factor in the initiation and progression of AD through a phenomenon of hysteresis with respect to the oligomer degradation rate .

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Viral infection develops in the organism due to virus replication inside infected cells and its transmission from infected to uninfected cells through the extracellular matrix or cell junctions. In this work, we model infection spreading in tissue with a delay reaction-diffusion system of equations for the concentrations of uninfected cells, infected cells and virus. We prove the wave existence, determine its speed of propagation and introduce a simplified one-equation model obtained from the complete model using a quasi-stationary approximation.

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We propose new single and two-strain epidemic models represented by systems of delay differential equations and based on the number of newly exposed individuals. Transitions between exposed, infectious, recovered, and back to susceptible compartments are determined by the corresponding time delays. Existence and positiveness of solutions are proved.

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We propose an epidemiological model for the interaction of either two viruses or viral strains with cross-immunity, where the individuals infected by the first virus cannot be infected by the second one, and without cross-immunity, where a secondary infection can occur. The model incorporates distributed recovery and death rates and consists of integro-differential equations governing the dynamics of susceptible, infectious, recovered, and dead compartments. Assuming that the recovery and death rates are uniformly distributed in time throughout the duration of the diseases, we can simplify the model to a conventional ordinary differential equation (ODE) model.

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Multiple myeloma (MM) is a genetically complex hematological cancer characterized by the abnormal proliferation of malignant plasma cells in the bone marrow. This disease progresses from a premalignant condition known as monoclonal gammopathy of unknown significance (MGUS) through sequential genetic alterations involving various genes. These genetic changes contribute to the uncontrolled growth of multiple clones of plasma cells.

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This article investigate a nonlocal reaction-diffusion system of equations modeling virus distribution with respect to their genotypes in the interaction with the immune response. This study demonstrates the existence of pulse solutions corresponding to virus quasi-species. The proof is based on the Leray-Schauder method, which relies on the topological degree for elliptic operators in unbounded domains and a priori estimates of solutions.

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We propose an epidemiological model with distributed recovery and death rates. It represents an integrodifferential system of equations for susceptible, exposed, infectious, recovered and dead compartments. This model can be reduced to the conventional ODE model under the assumption that recovery and death rates are uniformly distributed in time during disease duration.

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The emergence of new variants of concern (VOCs) of the SARS-CoV-2 infection is one of the main factors of epidemic progression. Their development can be characterized by three critical stages: virus mutation leading to the appearance of new viable variants; the competition of different variants leading to the production of a sufficiently large number of copies; and infection transmission between individuals and its spreading in the population. The first two stages take place at the individual level (infected individual), while the third one takes place at the population level with possible competition between different variants.

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In this work, we develop mathematical models of the immune response to respiratory viral infection, taking into account some particular properties of the SARS-CoV infections, cytokine storm and vaccination. Each model consists of a system of ordinary differential equations that describe the interactions of the virus, epithelial cells, immune cells, cytokines, and antibodies. Conventional analysis of the existence and stability of stationary points is completed by numerical simulations in order to study the dynamics of solutions.

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The work is devoted to a new immuno-epidemiological model with distributed recovery and death rates considered as functions of time after the infection onset. Disease transmission rate depends on the intra-subject viral load determined from the immunological submodel. The age-dependent model includes the viral load, recovery and death rates as functions of age considered as a continuous variable.

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Viral infection in cell culture and tissue is modeled with delay reaction-diffusion equations. It is shown that progression of viral infection can be characterized by the viral replication number, time-dependent viral load, and the speed of infection spreading. These three characteristics are determined through the original model parameters including the rates of cell infection and of virus production in the infected cells.

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Replication of viruses in living tissues and cell cultures is a "number game" involving complex biological processes (cell infection, virus replication inside infected cell, cell death, viral degradation) as well as transport processes limiting virus spatial propagation. In epithelial tissues and immovable cell cultures, viral particles are basically transported via Brownian diffusion. Highly non-linear kinetics of viral replication combined with diffusion limitation lead to spatial propagation of infection as a moving front switching from zero to high local viral concentration, the behavior typical of spatially distributed excitable media.

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A compartmental epidemiological model with distributed recovery and death rates is proposed. In some particular cases, the model can be reduced to the conventional SIR model. However, in general, the dynamics of epidemic progression in this model is different.

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Anticoagulant drugs are commonly prescribed to prevent hypercoagulable states in patients with venous thromboembolism. The choice of the most efficient anticoagulant and the appropriate dosage regimen remain a complex problem because of the intersubject variability in the coagulation kinetics and the effect of blood flow. The rapid assessment of the patient-specific response to anticoagulant regimens would assist clinical decision-making and ensure efficient management of coagulopathy.

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Platelet accumulation at the site of a vascular injury is regulated by soluble platelet agonists, which induce various types of platelet responses, including integrin activation and granule secretion. The interplay between local biochemical cues, mechanical interactions between platelets and macroscopic thrombus dynamics is poorly understood. Here we describe a novel computational model of microvascular clot formation for the detailed analysis of thrombus mechanics.

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Spatial distribution of the human population is distinctly heterogeneous, e.g. showing significant difference in the population density between urban and rural areas.

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In nature, different species compete among themselves for common resources and favorable habitat. Therefore, it becomes really important to determine the key factors in maintaining the bio-diversity. Also, some competing species follow cyclic competition in real world where the competitive dominance is characterized by a cyclic ordering.

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Damage to arterial vessel walls leads to the formation of platelet aggregate, which acts as a physical obstacle for bleeding. An arterial thrombus is heterogeneous; it has a dense inner part (core) and an unstable outer part (shell). The thrombus shell is very dynamic, being composed of loosely connected discoid platelets.

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An extended SEIQR type model is considered in order to model the COVID-19 epidemic. It contains the classes of susceptible individuals, exposed, infected symptomatic and asymptomatic, quarantined, hospitalized and recovered. The basic reproduction number and the final size of epidemic are determined.

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This paper represents a literature review on traveling waves described by delayed reactiondiffusion (RD, for short) equations. It begins with the presentation of different types of equations arising in applications. The main results on wave existence and stability are presented for the equations satisfying the monotonicity condition that provides the applicability of the maximum and comparison principles.

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This work deals with a reaction-diffusion model for prey-predator interaction with Bazykin's reaction kinetics and a nonlocal interaction term in prey growth. The kernel of the integral characterizes nonlocal consumption of resources and depends on space and time. Linear stability analysis determines the conditions of the emergence of Turing patterns without and with nonlocal term, while weakly nonlinear analysis allows the derivation of amplitude equations.

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Platelets upregulate the generation of thrombin and reinforce the fibrin clot which increases the incidence risk of venous thromboembolism (VTE). However, the role of platelets in the pathogenesis of venous cardiovascular diseases remains hard to quantify. An experimentally validated model of thrombin generation dynamics is formulated.

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Under voluntary vaccination, a critical role in shaping the level and trends of vaccine uptake is played by the type and structure of information that is received and used by parents of children eligible for vaccination. In this article we investigate the feedbacks of spatial mobility and the spatial structure of information on vaccination dynamics, by extending to a continuous spatially structured setting existing behavioral epidemiology models for the impact of vaccine adverse events (VAEs) on vaccination choices. We considered the simplest spatial setting, namely classical 'Fickian' diffusion, and focused on the noteworthy case where the infection is absent.

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