Publications by authors named "Abdessamad Tridane"

This research investigates a novel approach to modeling an SIR epidemic in a heterogeneous environment by imposing certain restrictions on population mobility. Our study reveals the influence of partially restricting the mobility of the infected population, who are allowed to diffuse locally and can be modeled using random dispersion. In contrast, the non-infective population, which includes susceptible and recovered individuals, has more freedom in their movements.

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This paper presents a comprehensive agent-based model for the spread of an infection in a network of cities. Directional mobility is defined between each two cities and can take different values. The work examines the role that such mobility levels play in containing the infection with various vaccination coverage and age distributions.

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Vaccination programs are crucial for reducing the prevalence of infectious diseases and ultimately eradicating them. A new age-structured SEIRV (S-Susceptible, E-Exposed, I-Infected, R-Recovered, V-Vaccinated) model with imperfect vaccination is proposed. After formulating our model, we show the existence and uniqueness of the solution using semigroup of operators.

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The world has faced the COVID-19 pandemic for over two years now, and it is time to revisit the lessons learned from lockdown measures for theoretical and practical epidemiological improvements. The interlink between these measures and the resulting change in mobility (a predictor of the disease transmission contact rate) is uncertain. We thus propose a new method for assessing the efficacy of various non-pharmaceutical interventions (NPI) and examine the aptness of incorporating mobility data for epidemiological modelling.

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With the increasing global adoption of COVID-19 vaccines, limitations on mass gathering events have started to gradually loosen. However, the large vaccine inequality recorded among different countries is an important aspect that policymakers must address when implementing control measures for such events. In this paper, we propose a model for the assessment of different control measures with the consideration of vaccine inequality in the population.

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This paper aims to investigate the global dynamics of an alcoholism epidemic model with distributed delays. The main feature of this model is that it includes the effect of the social pressure as a factor of drinking. As a result, our global stability is obtained without a "basic reproduction number" nor threshold condition.

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Given a discrete-time controlled bilinear systems with initial state and output function , we investigate the maximal output set Θ(Ω) = { ∈ ℝ , ∈ Ω, ∀ ≥ 0} where Ω is a given constraint set and is a subset of ℝ . Using some stability hypothesis, we show that Θ(Ω) can be determined via a finite number of inequations. Also, we give an algorithmic process to generate the set Θ(Ω).

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In this paper, we study a mathematical model investigating the impact of unreported cases of the COVID-19 in three North African countries: Algeria, Egypt, and Morocco. To understand how the population respects the restriction of population mobility implemented in each country, we use Google and Apple's mobility reports. These mobility reports help to quantify the effect of the population movement restrictions on the evolution of the active infection cases.

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As Malaria represents one of the major health burdens in Africa, there is a risk of reappearance of this vector-borne disease in malaria-free or low risk countries such as those in North Africa. One of the factors that can lead to this situation is the flow of sub-Saharan immigrants trying to reach Europe through North Africa. In this work, we investigate such a possibility via a mathematical model.

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This paper aims to study the global stability of an Ebola virus epidemic model. Although this epidemic ended in September 2015, it devastated several West African countries and mobilized the international community. With the recent cases of Ebola in the Democratic Republic of the Congo (DRC), the threat of the reappearance of this fatal disease remains.

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Thalassemia is a genetic blood disorder that causes abnormal hemoglobin. Hemoglobin is a protein in red blood cells that carries oxygen and is made of two proteins from four α-globin genes and two β-globin genes. A defect in one or more of these genes causes thalassemia.

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The aim of this work is to investigate a new mathematical model that describes the interactions between Hepatitis B virus (HBV), liver cells (hepatocytes), and the adaptive immune response. The qualitative analysis of this as cytotoxic T lymphocytes (CTL) cells and the antibodies. These outcomes are (1) a disease free steady state, which its local stability is characterized as usual by R (0) < 1, (2) and the existence of four endemic steady states when R (0) > 1.

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The aim of this work is to investigate the mechanisms involved in the clearance of viral infection of the influenza virus at the epithelium level by modeling and analyzing the interaction of the influenza virus specific cytotoxic T Lymphocytes (CTL cells) and the influenza virus infected epithelial cells. Since detailed and definite mechanisms that trigger CTL production and cell death are still debatable, we utilize two plausible mathematical models for the CTLs response to influenza infection (i) logistic growth and (ii) threshold growth. These models incorporate the simulating effect of the production of CTLs during the infection.

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A possible control strategy against the spread of an infectious disease is the treatment with antimicrobials that are given prophylactically to those who had a contact with an infective person. The treatment continues until recovery or until it becomes obvious that there was no infection in the first place. The model considers susceptible, treated uninfected exposed, treated infected, (untreated) infectious, and recovered individuals.

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We formulated a novel cellular automata (CA) model for HIV dynamics and drug treatment. The model is built upon realistic biological processes, including the virus replication cycle and mechanisms of drug therapy. Viral load, its effect on infection rate, and the role of latently infected cells in sustaining HIV infection are among the aspects that are explored and incorporated in the model.

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