Related papers: An epidemic model for an evolving pathogen with st…
As pathogens spread in a population of hosts, immunity is built up and the pool of susceptible individuals is depleted. This generates selective pressure, to which many human RNA viruses, such as influenza virus or SARS-CoV-2, respond with…
We study how the interplay between the memory immune response and pathogen mutation affects epidemic dynamics in two related models. The first explicitly models pathogen mutation and individual memory immune responses, with contacted…
A simple, but ``classical``, stochastic model for epidemic spread in a finite, but large, population is studied. The progress of the epidemic can be divided into three different phases that requires different tools to analyse. Initially the…
We introduce and discuss a minimal individual-based model for influenza dynamics. The model takes into account the effects of specific immunization against viral strains, but also infectivity randomness and the presence of a short-lived…
Epidemiological data on seasonal influenza show that the growth rate of the number of infected individuals can increase passing from one exponential growth rate to another one with a larger exponent. Such behavior is not described by…
Many infectious diseases are comprised of multiple strains with examples including Influenza, tuberculosis, and Dengue virus. The time evolution of such systems is linked to a complex landscape shaped by interactions between competing…
Several pathogens use evolvability as a survival strategy against acquired immunity of the host. Despite their high variability in time, some of them exhibit quite low variability within the population at any given time, a somehow…
The evolution of many microbes and pathogens, including circulating viruses such as seasonal influenza, is driven by immune pressure from the host population. In turn, the immune systems of infected populations get updated, chasing viruses…
Infectious disease outbreaks have precipitated a profusion of mathematical models. Epidemic curves predicted by these models are typically qualitatively similar, despite distinct model assumptions, but there is no theoretical explanation…
Epidemiological models for the spread of pathogens in a population are usually only able to describe a single pathogen. This makes their application unrealistic in cases where multiple pathogens with similar symptoms are spreading…
Mathematical disease modelling has long operated under the assumption that any one infectious disease is caused by one transmissible pathogen spreading among a population. This paradigm has been useful in simplifying the biological reality…
The spread of infectious disease and the evolution of antigenically distinct strains are often modeled separately, despite strong feedbacks mediated by host immune memory and heterogeneous contacts. To tackle this challenging problem, we…
The dynamics of epidemic spreading is often reduced to the single control parameter $R_0$, whose value, above or below unity, determines the state of the contagion. If, however, the pathogen evolves as it spreads, $R_0$ may change over…
Many pathogens spread primarily via direct contact between infected and susceptible hosts. Thus, the patterns of contacts or contact network of a population fundamentally shapes the course of epidemics. While there is a robust and growing…
We consider a spatial stochastic model for a pathogen population growing inside a host that attempts to eliminate the pathogens through its immune system. The pathogen population is divided into different types. A pathogen can either…
We consider a stochastic model for a pathogen population in the presence of an immune response, in which pathogen types are partially ordered by ancestry and the immune system must eliminate ancestor types before it can eliminate their…
Viruses evolve in the background of host immune systems that exert selective pressure and drive viral evolutionary trajectories. This interaction leads to different evolutionary patterns in antigenic space. Examples observed in nature…
Influenza viruses undergo continual antigenic evolution allowing mutant viruses to evade host immunity acquired to previous virus strains. Antigenic phenotype is often assessed through pairwise measurement of cross-reactivity between…
We consider a model for an influenza-like disease, in which, between seasons, the virus makes a random genetic drift $\delta$, (reducing immunity by the factor $\delta$) and obtains a new random transmissibility $\tau$ (closely related to…
We introduce and analyze coupled, multi-strain epidemic models designed to simulate the emergence and dissemination of mutant (e.g. drug-resistant) pathogen strains. In particular, we investigate the mathematical and biological properties…