The COVID-19 pandemic that started in China in December 2019 has not only threatened world public health, but severely impacted almost every facet of life, including behavioural and psychological aspects. In this paper, we focus on the ‘human element’ and propose a mathematical model to investigate the effects on the COVID-19 epidemic of social behavioural changes in response to lockdowns. We consider an SEIR-like epidemic model where the contact and quarantine rates depend on the available information and rumours about the disease status in the community. The model is applied to the case of the COVID-19 epidemic in Italy. We consider the period that stretches between 24 February 2020, when the first bulletin by the Italian Civil Protection was reported and 18 May 2020, when the lockdown restrictions were mostly removed. The role played by the information-related parameters is determined by evaluating how they affect suitable outbreak-severity indicators. We estimate that citizen compliance with mitigation measures played a decisive role in curbing the epidemic curve by preventing a duplication of deaths and about 46% more infections.

The viral load is known to be a chief predictor of the risk of transmission of infectious diseases. In this work, we investigate the role of the individuals’ viral load in the disease transmission by proposing a new susceptible-infectious-recovered epidemic model for the densities and mean viral loads of each compartment. To this aim, we formally derive the compartmental model from an appropriate microscopic one. Firstly, we consider a multi-agent system in which individuals are identified by the epidemiological compartment to which they belong and by their viral load. Microscopic rules describe both the switch of compartment and the evolution of the viral load. In particular, in the binary interactions between susceptible and infectious individuals, the probability for the susceptible individual to get infected depends on the viral load of the infectious individual. Then, we implement the prescribed microscopic dynamics in appropriate kinetic equations, from which the macroscopic equations for the densities and viral load momentum of the compartments are eventually derived. In the macroscopic model, the rate of disease transmission turns out to be a function of the mean viral load of the infectious population. We analytically and numerically investigate the case that the transmission rate linearly depends on the viral load, which is compared to the classical case of constant transmission rate. A qualitative analysis is performed based on stability and bifurcation theory. Finally, numerical investigations concerning the model reproduction number and the epidemic dynamics are presented.

In classical epidemic models, a neglected aspect is the heterogeneity of disease transmission and progression linked to the viral load of each infected individual. Here, we investigate the interplay between the evolution of individuals' viral load and the epidemic dynamics from a theoretical point of view. We propose a stochastic particle model describing the infection transmission and the individual physiological course of the disease. Agents have a double microscopic state: a discrete label, that denotes the epidemiological compartment to which they belong and switches in consequence of a Markovian process, and a microscopic trait, measuring their viral load, that changes in consequence of binary interactions or interactions with a background. Specifically, we consider Susceptible–Infected–Removed–like dynamics where infectious individuals may be isolated and the isolation rate may depend on the viral load–sensitivity and frequency of tests. We derive kinetic evolution equations for the distribution functions of the viral load of the individuals in each compartment, whence, via upscaling procedures, we obtain macroscopic equations for the densities and viral load momentum. We perform then a qualitative analysis of the ensuing macroscopic model. Finally, we present numerical tests in the case of both constant and viral load–dependent isolation control.