8,362 research outputs found
A minimal stochastic model for influenza evolution
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 strain transcending immunity recently suggested in the literature.
We show by simulations that the resulting model exhibits substitution of viral
strains along the years, but that their divergence remains bounded. We also
show that dropping any of these features results in a drastically different
behavior, leading either to the extinction of the disease, to the proliferation
of the viral strains, or to their divergence
Characterising two-pathogen competition in spatially structured environments
Different pathogens spreading in the same host population often generate
complex co-circulation dynamics because of the many possible interactions
between the pathogens and the host immune system, the host life cycle, and the
space structure of the population. Here we focus on the competition between two
acute infections and we address the role of host mobility and cross-immunity in
shaping possible dominance/co-dominance regimes. Host mobility is modelled as a
network of traveling flows connecting nodes of a metapopulation, and the
two-pathogen dynamics is simulated with a stochastic mechanistic approach.
Results depict a complex scenario where, according to the relation among the
epidemiological parameters of the two pathogens, mobility can either be
non-influential for the competition dynamics or play a critical role in
selecting the dominant pathogen. The characterisation of the parameter space
can be explained in terms of the trade-off between pathogen's spreading
velocity and its ability to diffuse in a sparse environment. Variations in the
cross-immunity level induce a transition between presence and absence of
competition. The present study disentangles the role of the relevant biological
and ecological factors in the competition dynamics, and provides relevant
insights into the spatial ecology of infectious diseases.Comment: 30 pages, 6 figures, 1 table. Final version accepted for publication
in Scientific Report
Human mobility networks and persistence of rapidly mutating pathogens
Rapidly mutating pathogens may be able to persist in the population and reach
an endemic equilibrium by escaping hosts' acquired immunity. For such diseases,
multiple biological, environmental and population-level mechanisms determine
the dynamics of the outbreak, including pathogen's epidemiological traits (e.g.
transmissibility, infectious period and duration of immunity), seasonality,
interaction with other circulating strains and hosts' mixing and spatial
fragmentation. Here, we study a susceptible-infected-recovered-susceptible
model on a metapopulation where individuals are distributed in subpopulations
connected via a network of mobility flows. Through extensive numerical
simulations, we explore the phase space of pathogen's persistence and map the
dynamical regimes of the pathogen following emergence. Our results show that
spatial fragmentation and mobility play a key role in the persistence of the
disease whose maximum is reached at intermediate mobility values. We describe
the occurrence of different phenomena including local extinction and emergence
of epidemic waves, and assess the conditions for large scale spreading.
Findings are highlighted in reference to previous works and to real scenarios.
Our work uncovers the crucial role of hosts' mobility on the ecological
dynamics of rapidly mutating pathogens, opening the path for further studies on
disease ecology in the presence of a complex and heterogeneous environment.Comment: 29 pages, 7 figures. Submitted for publicatio
How the other half lives: CRISPR-Cas's influence on bacteriophages
CRISPR-Cas is a genetic adaptive immune system unique to prokaryotic cells
used to combat phage and plasmid threats. The host cell adapts by incorporating
DNA sequences from invading phages or plasmids into its CRISPR locus as
spacers. These spacers are expressed as mobile surveillance RNAs that direct
CRISPR-associated (Cas) proteins to protect against subsequent attack by the
same phages or plasmids. The threat from mobile genetic elements inevitably
shapes the CRISPR loci of archaea and bacteria, and simultaneously the
CRISPR-Cas immune system drives evolution of these invaders. Here we highlight
our recent work, as well as that of others, that seeks to understand phage
mechanisms of CRISPR-Cas evasion and conditions for population coexistence of
phages with CRISPR-protected prokaryotes.Comment: 24 pages, 8 figure
Severe population collapses and species extinctions in multi-host epidemic dynamics
Most infectious diseases including more than half of known human pathogens
are not restricted to just one host, yet much of the mathematical modeling of
infections has been limited to a single species. We investigate consequences of
a single epidemic propagating in multiple species and compare and contrast it
with the endemic steady state of the disease. We use the two-species
Susceptible-Infected-Recovered (SIR) model to calculate the severity of
post-epidemic collapses in populations of two host species as a function of
their initial population sizes, the times individuals remain infectious, and
the matrix of infection rates. We derive the criteria for a very large,
extinction-level, population collapse in one or both of the species. The main
conclusion of our study is that a single epidemic could drive a species with
high mortality rate to local or even global extinction provided that it is
co-infected with an abundant species. Such collapse-driven extinctions depend
on factors different than those in the endemic steady state of the disease
The epidemiological consequences of optimisation of the individual host immune response
We present a simple unscaled, quantitative framework that addresses the optimum use of resources throughout a host's lifetime based on continuous exposure to parasites (rather than evolutionary, genetically explicit trade-offs). The principal assumptions are that a host's investment of resources in growth increases its survival and reproduction, and that increasing parasite burden reduces survival. The host reproductive value is maximised for a given combination of rates of parasite exposure, host resource acquisition and pathogenicity, which results in an optimum parasite burden (for the host). Generally, results indicate that the optimum resource allocation is to tolerate some parasite infection. The lower the resource acquisition, the lower the proportion of resources that should be devoted to immunity, i.e. the higher the optimum parasite burden. Increases in pathogenicity result in reduced optimum parasite burdens, whereas increases in exposure result in increasing optimum parasite burdens. Simultaneous variation in resource acquisition, pathogenicity and exposure within a community of hosts results in overdispersed parasite burdens, with the degree of heterogeneity decreasing as mean burden increases. The relationships between host condition and parasite burden are complicated, and could potentially confound data analysis. Finally, the value of this approach for explaining epidemiological patterns, immunological processes and the possibilities for further work are discussed
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