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Julien Arino

Publications and source records attributed to Julien Arino.

10 recordsLinked to original sources

A model with exposure in the epidemiological sense. Part 1 -- Base model

We explore a model of infectious disease spread that incorporates exposure to the pathogen in the classic epidemiological acceptation of the term, i.e., a contact with an infectious individual has taken place but the infection has not necessarily been acquired. The model also includes a (discrete) age of infection structure, allowing to implicitly describe the viral load of infected individuals and in turn, to describe the probability of developing an infection as a function of the viral load of the infectious contacts.

q-bio.PE

Dose-limited interventions in an epidemiological model

We consider an SLIARS mathematical epidemiology model including intervention in the form of vaccination and treatment. Contrary to classical models, it is assumed that treatment doses can be limited in availability. Mathematically, we show that most scenarios actually reduce to classic well-known scenarios: having an unreplenished number of doses is akin to having none, while being able to restore stocks is (often) equivalent to the classic situation with vaccination and treatment. We also perform a computational analysis, illustrating some of the transient and stochastic dynamics that diverge from deterministic long-term behaviour, as well as the impact of budgetary constraints.

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Within-host immunology to age-of-infection epidemiology via a virtual cohort

We present a methodology providing a one-directional link from within-host individual heterogeneity to population-level disease transmission dynamics. The methodology works in several steps. A within-host model is investigated numerically to determine pathogen and immunological parameters leading to the largest variation of model responses. These key parameters are used to generate a synthetic population of individuals whose temporal immunological response profiles are recorded. These responses are ranked in terms of the severity of experienced outcomes, from mild infections to death, as a function of time since infection. This is used to parametrise an age-of-infection structured epidemiological model to study the transmission dynamics of the disease at the population level. The approach is illustrated using a within-host model describing SARS-CoV-2 infection and an SIR population-level model.

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Deterministic and stochastic infection dynamics in a population subject to stress

Physiological stress fundamentally alters disease susceptibility in aquatic environments. In this paper, we develop a stress-structured epidemiological model where host vulnerability is dynamically driven by water quality. Analytically, we establish that the system exhibits a classic forward bifurcation at $\mathcal{R}_0=1$, confirming that the basic reproduction number remains a valid threshold for eradication. However, stochastic analysis reveals a critical asymmetry not captured by deterministic thresholds. We show that while $\mathcal{R}_0$ predicts stability, the probability of an outbreak depends on the initial physiological state. Introducing infection into a stressed sub-population leads to immediate rapid growth of the disease, whereas introduction into the normal class faces a stochastic barrier that significantly delays the epidemic peak.

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A metapopulation model for the spread of cholera

We consider a metapopulation model of cholera describing explicitly the movement of individuals and contaminated water between locations as well as a simple vaccination mechanism. The global stability of the disease-free equilibrium point when the location-specific reproduction numbers are all less than unity is established. We then conduct some numerical investigation of the model.

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A model for cholera with infectiousness of deceased individuals and vaccination

A cholera transmission model is formulated that incorporates water-borne and horizontal transmissions as well as infectivity of deceased individuals. The model includes an Allee effect for the bacteria in the environment and imperfect and waning vaccination. Mathematical properties of the model are investigated, with an environmental bistability shown to combine with a vaccine-driven one, although a computational search for the latter fails to detect its presence in realistic parameter ranges. The computational analysis also considers the interplay between vaccination strategy, vaccine efficacy and waning, as well as the effect of transmission of the disease during funeral rites. The effect of control scenarios such as WASH or Safe and dignified burials are assessed.

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Threshold-based impulsive biocontrol for coffee leaf rust

Coffee leaf rust (CLR) severely affects coffee production worldwide, leading to reduced yields and economic losses. To reduce the cost of control, small-scale farmers often only apply control measures once a noticeable level of infection is reached. In this work, we develop mathematical models to better understand CLR dynamics and impulsive biocontrol with threshold-based interventions. We first use ordinary and impulsive differential equations to describe disease spread and the application of control measures once a certain infection level is detected. These models help determine when and how often interventions should occur. To capture the early stages of the disease and the chance that it might die out by itself, we then use a continuous-time Markov chain approach. This stochastic model allows us to estimate the probability that the pathogen fails to establish, thereby avoiding serious outbreaks.

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Transmission of multiple pathogens across species

We analyse a model that describes the propagation of many pathogens within and between many species. A branching process approximation is used to compute the probability of disease outbreaks. Special cases of aquatic environments with two host species and one or two pathogens are considered both analytically and computationally.

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Mathematical modelling of the first HIV/ZIKV co-infection cases in Colombia and Brazil

This paper presents a mathematical model to investigate co-infection with HIV/AIDS and zika virus (ZIKV) in Colombia and Brazil, where the first cases were reported in 2015-2016. The model considers the sexual transmission dynamics of both viruses and vector-host interactions. We begin by exploring the qualitative behaviour of each model separately. Then, we analyze the dynamics of the co-infection model using the thresholds and results defined separately for each model. The model also considers the impact of intervention strategies, such as, personal protection, antiretroviral therapy (ART), and sexual protection (condoms use). Using available parameter values for Colombia and Brazil, the model is calibrated to predict the potential effect of implementing combinations of those intervention strategies on the co-infection spread. According to these findings, transmission through sexual contact is a determining factor in the long-term behaviour of these two diseases. Furthermore, it is important to note that co-infection with HIV and ZIKV may result in higher rates of HIV transmission and an increased risk of severe congenital disabilities linked to ZIKV infection. As a result, control measures have been implemented to limit the number of infected individuals and mosquitoes, with the aim of halting disease transmission. This study provides novel insights into the dynamics of HIV/ZIKV co-infection and highlights the importance of integrated intervention strategies in controlling the spread of these viruses, which may impact public health

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