9,707 research outputs found
The role of spatial heterogeneity in the evolution of local and global infections of viruses
Viruses have two modes spread in a host body, one is to release infectious particles from infected cells (global infection) and the other is to infect directly from an infected cell to an adjacent cell (local infection). Since the mode of spread affects the evolution of life history traits, such as virulence, it is important to reveal what level of global and local infection is selected. Previous studies of the evolution of global and local infection have paid little attention to its dependency on the measures of spatial configuration. Here we show the evolutionarily stable proportion of global and local infection, and how it depends on the distribution of target cells. Using an epidemic model on a regular lattice, we consider the infection dynamics by pair approximation and check the evolutionarily stable strategy. We also conduct the Monte-Carlo simulation to observe evolutionary dynamics. We show that a higher local infection is selected as target cells become clustered. Surprisingly, the selected strategy depends not only on the degree of clustering but also the abundance of target cells per se
Integrating the landscape epidemiology and genetics of RNA viruses: rabies in domestic dogs as a model
Landscape epidemiology and landscape genetics combine advances in molecular techniques, spatial analyses and epidemiological models to generate a more real-world understanding of infectious disease dynamics and provide powerful new tools for the study of RNA viruses. Using dog rabies as a model we have identified how key questions regarding viral spread and persistence can be addressed using a combination of these techniques. In contrast to wildlife rabies, investigations into the landscape epidemiology of domestic dog rabies requires more detailed assessment of the role of humans in disease spread, including the incorporation of anthropogenic landscape features, human movements and socio-cultural factors into spatial models. In particular, identifying and quantifying the influence of anthropogenic features on pathogen spread and measuring the permeability of dispersal barriers are important considerations for planning control strategies, and may differ according to cultural, social and geographical variation across countries or continents. Challenges for dog rabies research include the development of metapopulation models and transmission networks using genetic information to uncover potential source/sink dynamics and identify the main routes of viral dissemination. Information generated from a landscape genetics approach will facilitate spatially strategic control programmes that accommodate for heterogeneities in the landscape and therefore utilise resources in the most cost-effective way. This can include the efficient placement of vaccine barriers, surveillance points and adaptive management for large-scale control programmes
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
On the Dynamics of Dengue Virus type 2 with Residence Times and Vertical Transmission
A two-patch mathematical model of Dengue virus type 2 (DENV-2) that accounts
for vectors' vertical transmission and between patches human dispersal is
introduced. Dispersal is modeled via a Lagrangian approach. A host-patch
residence-times basic reproduction number is derived and conditions under which
the disease dies out or persists are established. Analytical and numerical
results highlight the role of hosts' dispersal in mitigating or exacerbating
disease dynamics. The framework is used to explore dengue dynamics using, as a
starting point, the 2002 outbreak in the state of Colima, Mexico
Nephropathia epidemica and Puumala virus occurrence in relation to bank vole (Clethrionomys glareolus) dynamics and environmental factors in northern Sweden
The objectives of the thesis were to investigate the spatio-temporal patterns of nephropathia epidemica (NE) in humans and Puumala virus (PUU) occurrence in relation to bank vole (Clethrionomys glareolus) dynamics and environmental factors in a region of high incidence of NE in northern Sweden. Nephropathia epidemica is a mild form of hemorrhagic fever with renal syndrome, and in northern Sweden the most prevailing serious febrile viral infection, second to influenza. All serologically confirmed NE cases during 1991-2001 in the four northernmost counties (n = 2,468) were used to establish spatio-temporal patterns of the occurrence of the human disease. Within the study region, the bank voles show marked population fluctuations with 3-4 yr cycles and the incidence of NE has a temporal component strongly correlated to annual numbers of bank voles in autumn. People living in rural dwellings near coastal areas were abundant among notified cases and middle-aged males were over-represented. The patients were often infected in autumn when engaged in activities such as handling of fire wood, gardening or hay-handling near man-made rodent refugia or cleaning/redecorating within one. A proportion of these patients, confident about site of PUU exposure, were used to establish field sites in two separate studies. Firstly a five year study (1995-1999) at six sites spanning a bank vole population cycle, and secondly a spatially extensive study at 32 sites was conducted in autumn 1998. Densities, fluctuations and demography of vole populations differ between sites of known occurrence of NE were compared to random forest sites. Five years of repeated biannual sampling revealed that case sites harbored more bank voles than random forest sites, in particular during population peaks. For the individual bank voles, the probability of PUU infection was significantly higher in population peak year, increased with age and was higher for males than for females. In the spatially extended study, it was found that in particular environmental characteristics associated with old-growth moist forests (i.e. Alectoria spp., Picea abies, fallen wood and Vaccinium myrtillus) were associated with high bank vole numbers and numbers of PUU infected bank voles. This implies that success in circulation and persistence of PUU within local bank vole populations is strongly influenced by the local environments. In future modeling of PUU transmission, influence of bank vole demography and environmental factors should be useful on establishing risk assessments and identifying areas of particular risk of PUU exposure
Immunization of complex networks
Complex networks such as the sexual partnership web or the Internet often
show a high degree of redundancy and heterogeneity in their connectivity
properties. This peculiar connectivity provides an ideal environment for the
spreading of infective agents. Here we show that the random uniform
immunization of individuals does not lead to the eradication of infections in
all complex networks. Namely, networks with scale-free properties do not
acquire global immunity from major epidemic outbreaks even in the presence of
unrealistically high densities of randomly immunized individuals. The absence
of any critical immunization threshold is due to the unbounded connectivity
fluctuations of scale-free networks. Successful immunization strategies can be
developed only by taking into account the inhomogeneous connectivity properties
of scale-free networks. In particular, targeted immunization schemes, based on
the nodes' connectivity hierarchy, sharply lower the network's vulnerability to
epidemic attacks
Modelling the species jump: towards assessing the risk of human infection from novel avian influenzas
The scientific understanding of the driving factors behind zoonotic and pandemic influenzas is hampered by complex interactions between viruses, animal hosts and humans. This complexity makes identifying influenza viruses of high zoonotic or pandemic risk, before they emerge from animal populations, extremely difficult and uncertain. As a first step towards assessing zoonotic risk of Influenza, we demonstrate a risk assessment framework to assess the relative likelihood of influenza A viruses, circulating in animal populations, making the species jump into humans. The intention is that such a risk assessment framework could assist decisionmakers to compare multiple influenza viruses for zoonotic potential and hence to develop appropriate strain-specific control measures. It also provides a first step towards showing proof of principle for an eventual pandemic risk model. We show that the spatial and temporal epidemiology is as important in assessing the risk of an influenza A species jump as understanding the innate molecular capability of the virus.We also demonstrate data deficiencies that need to be addressed in order to consistently combine both epidemiological and molecular virology data into a risk assessment framework
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