A Spatial Kinetic Model of Crowd Evacuation Dynamics with Infectious Disease Contagion.

This paper proposes a kinetic theory approach coupling together the modeling of crowd evacuation from a bounded domain with exit doors and infectious disease contagion. The spatial movement of individuals in the crowd is modeled by a proper description of the interactions with people in the crowd and the environment, including walls and exits. At the same time, interactions among healthy and infectious individuals may generate disease spreading if exposure time is long enough. Immunization of the population and individual awareness to contagion is considered as well. Interactions are modeled by tools of game theory, that let us propose the so-called tables of games that are introduced in the general kinetic equations. The proposed model is qualitatively studied and, through a series of case studies, we explore different scenarios related to crowding and gathering formation within indoor venues under the spread of a respiratory infectious disease, obtaining insights on specific policies to reduce contagion that may be implemented.

Mathematical models for dengue fever epidemiology: A 10-year systematic review.

Mathematical models have a long history in epidemiological research, and as the COVID-19 pandemic progressed, research on mathematical modeling became imperative and very influential to understand the epidemiological dynamics of disease spreading. Mathematical models describing dengue fever epidemiological dynamics are found back from 1970. Dengue fever is a viral mosquito-borne infection caused by four antigenically related but distinct serotypes (DENV-1 to DENV-4). With 2.5 billion people at risk of acquiring the infection, it is a major international public health concern. Although most of the cases are asymptomatic or mild, the disease immunological response is complex, with severe disease linked to the antibody-dependent enhancement (ADE) - a disease augmentation phenomenon where pre-existing antibodies to previous dengue infection do not neutralize but rather enhance the new infection. Here, we present a 10-year systematic review on mathematical models for dengue fever epidemiology. Specifically, we review multi-strain frameworks describing host-to-host and vector-host transmission models and within-host models describing viral replication and the respective immune response. Following a detailed literature search in standard scientific databases, different mathematical models in terms of their scope, analytical approach and structural form, including model validation and parameter estimation using empirical data, are described and analyzed. Aiming to identify a consensus on infectious diseases modeling aspects that can contribute to public health authorities for disease control, we revise the current understanding of epidemiological and immunological factors influencing the transmission dynamics of dengue. This review provide insights on general features to be considered to model aspects of real-world public health problems, such as the current epidemiological scenario we are living in.

Modeling Dengue Immune Responses Mediated by Antibodies: A Qualitative Study.

Dengue fever is a viral mosquito-borne infection and a major international public health concern. With 2.5 billion people at risk of acquiring the infection around the world, disease severity is influenced by the immunological status of the individual, seronegative or seropositive, prior to natural infection. Caused by four antigenically related but distinct serotypes, DENV-1 to DENV-4, infection by one serotype confers life-long immunity to that serotype and a period of temporary cross-immunity (TCI) to other serotypes. The clinical response on exposure to a second serotype is complex with the so-called antibody-dependent enhancement (ADE) process, a disease augmentation phenomenon when pre-existing antibodies to previous dengue infection do not neutralize but rather enhance the new infection, used to explain the etiology of severe disease. In this paper, we present a minimalistic mathematical model framework developed to describe qualitatively the dengue immunological response mediated by antibodies. Three models are analyzed and compared: (i) primary dengue infection, (ii) secondary dengue infection with the same (homologous) dengue virus and (iii) secondary dengue infection with a different (heterologous) dengue virus. We explore the features of viral replication, antibody production and infection clearance over time. The model is developed based on body cells and free virus interactions resulting in infected cells activating antibody production. Our mathematical results are qualitatively similar to the ones described in the empiric immunology literature, providing insights into the immunopathogenesis of severe disease. Results presented here are of use for future research directions to evaluate the impact of dengue vaccines.

Critical fluctuations in epidemic models explain COVID-19 post-lockdown dynamics.

As the COVID-19 pandemic progressed, research on mathematical modeling became imperative and very influential to understand the epidemiological dynamics of disease spreading. The momentary reproduction ratio r(t) of an epidemic is used as a public health guiding tool to evaluate the course of the epidemic, with the evolution of r(t) being the reasoning behind tightening and relaxing control measures over time. Here we investigate critical fluctuations around the epidemiological threshold, resembling new waves, even when the community disease transmission rate [Formula: see text] is not significantly changing. Without loss of generality, we use simple models that can be treated analytically and results are applied to more complex models describing COVID-19 epidemics. Our analysis shows that, rather than the supercritical regime (infectivity larger than a critical value, [Formula: see text]) leading to new exponential growth of infection, the subcritical regime (infectivity smaller than a critical value, [Formula: see text]) with small import is able to explain the dynamic behaviour of COVID-19 spreading after a lockdown lifting, with [Formula: see text] hovering around its threshold value.

A multiscale model of virus pandemic: Heterogeneous interactive entities in a globally connected world.

This paper is devoted to the multidisciplinary modelling of a pandemic initiated by an aggressive virus, specifically the so-called SARS-CoV-2 Severe Acute Respiratory Syndrome, corona virus n.2. The study is developed within a multiscale framework accounting for the interaction of different spatial scales, from the small scale of the virus itself and cells, to the large scale of individuals and further up to the collective behaviour of populations. An interdisciplinary vision is developed thanks to the contributions of epidemiologists, immunologists and economists as well as those of mathematical modellers. The first part of the contents is devoted to understanding the complex features of the system and to the design of a modelling rationale. The modelling approach is treated in the second part of the paper by showing both how the virus propagates into infected individuals, successfully and not successfully recovered, and also the spatial patterns, which are subsequently studied by kinetic and lattice models. The third part reports the contribution of research in the fields of virology, epidemiology, immune competition, and economy focussed also on social behaviours. Finally, a critical analysis is proposed looking ahead to research perspectives.