arXiv subjects

Chiara Poletto

Publications and source records attributed to Chiara Poletto.

At least 19 recordsLinked to original sources

arXiv2019

Interplay between competitive and cooperative interactions in a three-player pathogen system

In ecological systems heterogeneous interactions between pathogens take place simultaneously. This occurs, for instance, when two pathogens cooperate, while at the same time multiple strains of these pathogens co-circulate and compete. Notable examples include the cooperation of HIV with antibiotic-resistant and susceptible strains of tuberculosis, or some respiratory infections with Streptococcus pneumoniae strains. Models focusing on competition or cooperation separately fail to describe how these concurrent interactions shape the epidemiology of such diseases. We studied this problem considering two cooperating pathogens, where one pathogen is further structured in two strains. The spreading follows a susceptible-infected-susceptible process and the strains differ in transmissibility and extent of cooperation with the other pathogen. We combined a mean-field stability analysis with stochastic simulations on networks considering both well-mixed and structured populations. We observed the emergence of a complex phase diagram, where the conditions for the less transmissible, but more cooperative strain to dominate are non-trivial, e.g. non-monotonic boundaries and bistability. Coupled with community structure, the presence of the cooperative pathogen enables the co-existence between strains by breaking the spatial symmetry and dynamically creating different ecological niches. These results shed light on ecological mechanisms that may impact the epidemiology of diseases of public health concern.

q-bio.PE↗

arXiv2018

Dynamics of new strain emergence on a temporal network

Multi-strain competition on networks is observed in many contexts, including infectious disease ecology, information dissemination or behavioral adaptation to epidemics. Despite a substantial body of research has been developed considering static, time-aggregated networks, it remains a challenge to understand the transmission of concurrent strains when links of the network are created and destroyed over time. Here we analyze how network dynamics shapes the outcome of the competition between an initially endemic strain and an emerging one, when both strains follow a susceptible-infected-susceptible dynamics, and spread at time scales comparable with the network evolution one. Using time-resolved data of close-proximity interactions between patients admitted to a hospital and medical health care workers, we analyze the impact of temporal patterns and initial conditions on the dominance diagram and coexistence time. We find that strong variations in activity volume cause the probability that the emerging strain replaces the endemic one to be highly sensitive to the time of emergence. The temporal structure of the network shapes the dominance diagram, with significant variations in the replacement probability (for a given set of epidemiological parameters) observed from the empirical network and a randomized version of it. Our work contributes towards the description of the complex interplay between competing pathogens on temporal networks.

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arXiv2018

Epidemic Threshold in Continuous-Time Evolving Networks

Current understanding of the critical outbreak condition on temporal networks relies on approximations (time scale separation, discretization) that may bias the results. We propose a theoretical framework to compute the epidemic threshold in continuous time through the infection propagator approach. We introduce the {\em weak commutation} condition allowing the interpretation of annealed networks, activity-driven networks, and time scale separation into one formalism. Our work provides a coherent connection between discrete and continuous time representations applicable to realistic scenarios.

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arXiv2016

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.

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arXiv2016

Impact of spatially constrained sampling of temporal contact networks on the evaluation of the epidemic risk

The ability to directly record human face-to-face interactions increasingly enables the development of detailed data-driven models for the spread of directly transmitted infectious diseases at the scale of individuals. Complete coverage of the contacts occurring in a population is however generally unattainable, due for instance to limited participation rates or experimental constraints in spatial coverage. Here, we study the impact of spatially constrained sampling on our ability to estimate the epidemic risk in a population using such detailed data-driven models. The epidemic risk is quantified by the epidemic threshold of the susceptible-infectious-recovered-susceptible model for the propagation of communicable diseases, i.e. the critical value of disease transmissibility above which the disease turns endemic. We verify for both synthetic and empirical data of human interactions that the use of incomplete data sets due to spatial sampling leads to the underestimation of the epidemic risk. The bias is however smaller than the one obtained by uniformly sampling the same fraction of contacts: it depends nonlinearly on the fraction of contacts that are recorded and becomes negligible if this fraction is large enough. Moreover, it depends on the interplay between the timescales of population and spreading dynamics.

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arXiv2015

Infection propagator approach to compute epidemic thresholds on temporal networks: impact of immunity and of limited temporal resolution

The epidemic threshold of a spreading process indicates the condition for the occurrence of the wide spreading regime, thus representing a predictor of the network vulnerability to the epidemic. Such threshold depends on the natural history of the disease and on the pattern of contacts of the network with its time variation. Based on the theoretical framework introduced in (Valdano et al. PRX 2015) for a susceptible-infectious-susceptible model, we formulate here an infection propagator approach to compute the epidemic threshold accounting for more realistic effects regarding a varying force of infection per contact, the presence of immunity, and a limited time resolution of the temporal network. We apply the approach to two temporal network models and an empirical dataset of school contacts. We find that permanent or temporary immunity do not affect the estimation of the epidemic threshold through the infection propagator approach. Comparisons with numerical results show the good agreement of the analytical predictions. Aggregating the temporal network rapidly deteriorates the predictions, except for slow diseases once the heterogeneity of the links is preserved. Weight-topology correlations are found to be the critical factor to be preserved to improve accuracy in the prediction.

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arXiv2015

Analytical computation of the epidemic threshold on temporal networks

The time variation of contacts in a networked system may fundamentally alter the properties of spreading processes and affect the condition for large-scale propagation, as encoded in the epidemic threshold. Despite the great interest in the problem for the physics, applied mathematics, computer science and epidemiology communities, a full theoretical understanding is still missing and currently limited to the cases where the time-scale separation holds between spreading and network dynamics or to specific temporal network models. We consider a Markov chain description of the Susceptible-Infectious-Susceptible process on an arbitrary temporal network. By adopting a multilayer perspective, we develop a general analytical derivation of the epidemic threshold in terms of the spectral radius of a matrix that encodes both network structure and disease dynamics. The accuracy of the approach is confirmed on a set of temporal models and empirical networks and against numerical results. In addition, we explore how the threshold changes when varying the overall time of observation of the temporal network, so as to provide insights on the optimal time window for data collection of empirical temporal networked systems. Our framework is both of fundamental and practical interest, as it offers novel understanding of the interplay between temporal networks and spreading dynamics.

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arXiv2015

Predicting epidemic risk from past temporal contact data

Understanding how epidemics spread in a system is a crucial step to prevent and control outbreaks, with broad implications on the system's functioning, health, and associated costs. This can be achieved by identifying the elements at higher risk of infection and implementing targeted surveillance and control measures. One important ingredient to consider is the pattern of disease-transmission contacts among the elements, however lack of data or delays in providing updated records may hinder its use, especially for time-varying patterns. Here we explore to what extent it is possible to use past temporal data of a system's pattern of contacts to predict the risk of infection of its elements during an emerging outbreak, in absence of updated data. We focus on two real-world temporal systems; a livestock displacements trade network among animal holdings, and a network of sexual encounters in high-end prostitution. We define the node's loyalty as a local measure of its tendency to maintain contacts with the same elements over time, and uncover important non-trivial correlations with the node's epidemic risk. We show that a risk assessment analysis incorporating this knowledge and based on past structural and temporal pattern properties provides accurate predictions for both systems. Its generalizability is tested by introducing a theoretical model for generating synthetic temporal networks. High accuracy of our predictions is recovered across different settings, while the amount of possible predictions is system-specific. The proposed method can provide crucial information for the setup of targeted intervention strategies.

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arXiv2014

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.

q-bio.PE↗

arXiv2014

Regional spread of chikungunya fever in the Americas

Chikungunya fever (CHIKV), a viral disease transmitted by mosquitoes, is currently affecting several territories in the Caribbean. The vector is found in the Americas from South Florida to Brazil and the Caribbean is a highly connected region. There is therefore a significant risk for the epidemic to quickly expand to a wide area in the Americas, and of introduction to Europe where competent vectors are present. Here, we describe the spread of CHIKV in the first three territories to report cases and between territories of the region. Local transmission of CHIKV in the Caribbean is found to be very effective (mean number of cases generated by a human case in the range 2 to 4). There is a strong spatial signature in the regional epidemic, with the risk of transmission between territories estimated to be inversely proportional to the distance rather than being driven by air transportation. So far, this simple model has successfully predicted observed patterns of spread. The spatial structure allows ranking territories according to their current risk of invasion. This characterization may help national and international agencies to optimize resource allocation for monitoring and control and encourage territories with elevated risks to act. This is important to reduce the risk of dissemination to other parts of the world, including Europe.

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arXiv2014

Assessment of the MERS-CoV epidemic situation in the Middle East region

The appearance of a novel coronavirus named Middle East (ME) Respiratory Syndrome Coronavirus (MERS-CoV) has raised global public health concerns regarding the current situation and its future evolution. Here we propose an integrative maximum likelihood analysis of both cluster data in the ME region and importations in Europe to assess transmission scenario and incidence of sporadic infections. Our approach is based on a spatial-transmission model integrating mobility data worldwide and allows for variations in the zoonotic/environmental transmission and underascertainment. Maximum likelihood estimates for the ME region indicate the occurrence of a subcritical epidemic (R=0.50, 95% confidence interval (CI) 0.30-0.77) associated with a 0.28 (95% CI 0.12-0.85) daily rate of sporadic introductions. Infections in the region appear to be mainly dominated by zoonotic/environmental transmissions, with possible underascertainment (95% CI of estimated to observed sporadic cases in the range 1.03-7.32). No time evolution of the situation emerges. Analyses of flight passenger data from the region indicate areas at high risk of importation. While dismissing an immediate threat for global health security, this analysis provides a baseline scenario for future reference and updates, suggests reinforced surveillance to limit underascertainment, and calls for increased alertness in high-risk areas worldwide.

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arXiv2014

Metapopulation epidemic models with heterogeneous mixing and travel behaviour

The complex interplay between population movements in space and non-homogeneous mixing patterns have so far hindered the fundamental understanding of the conditions for spatial invasion through a general theoretical framework. To address this issue, we present an analytical modelling approach taking into account such interplay under general conditions of mobility and interactions, in the simplifying assumption of two population classes. We describe a spatially structured population with non-homogeneous mixing and travel behaviour through a multi-host stochastic epidemic metapopulation model. Different population partitions, mixing patterns and mobility structures are considered, along with a specific application for the study of the role of age partition in the early spread of the 2009 H1N1 pandemic influenza. We provide a complete mathematical formulation of the model and derive a semi-analytical expression of the threshold condition for global invasion of an emerging infectious disease in the metapopulation system. A rich solution space is found that depends on the social partition of the population, the pattern of contacts across groups and their relative social activity, the travel attitude of each class, and the topological and traffic features of the mobility network. Reducing the activity of the less social group and reducing the cross-group mixing are predicted to be the most efficient strategies for controlling the pandemic potential in the case the less active group constitutes the majority of travellers. If instead traveling is dominated by the more social class, our model predicts the existence of an optimal across-groups mixing that maximises the pandemic potential of the disease, whereas the impact of variations in the activity of each group is less important.

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arXiv2013

Human mobility and time spent at destination: Impact on spatial epidemic spreading

Host mobility plays a fundamental role in the spatial spread of infectious diseases. Previous theoretical works based on the integration of network theory into the metapopulation framework have shown that the heterogeneities that characterize real mobility networks favor the propagation of epidemics. Nevertheless, the studies conducted so far assumed the mobility process to be either Markovian or non-Markovian with a fixed traveling time scale. Available statistics however show that the time spent by travelers at destination is characterized by wide fluctuations, ranging between a single day up to several months. Such varying length of stay crucially affects the chance and duration of mixing events among hosts and may therefore have a strong impact on the spread of an emerging disease. Here, we present an analytical and computational study of epidemic processes on a complex subpopulation network where travelers have memory of their origin and spend a heterogeneously distributed time interval at their destination. Through analytical calculations and numerical simulations we show that the heterogeneity of the length of stay alters the expression of the threshold between local outbreak and global invasion, and, moreover, it changes the epidemic behavior of the system in case of a global outbreak. Additionally, our theoretical framework allows us to study the effect of changes in the traveling behavior in response to the infection, by considering a scenario in which sick individuals do not leave their home location. Finally, we compare the results of our non-Markovian framework with those obtained with a classic Markovian approach and find relevant differences between the two, in the estimate of the epidemic invasion potential, as well as of the timing and the pattern of its spatial spread.

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arXiv2013

Host mobility drives pathogen competition in spatially structured populations

Interactions among multiple infectious agents are increasingly recognized as a fundamental issue in the understanding of key questions in public health, regarding pathogen emergence, maintenance, and evolution. The full description of host-multipathogen systems is however challenged by the multiplicity of factors affecting the interaction dynamics and the resulting competition that may occur at different scales, from the within-host scale to the spatial structure and mobility of the host population. Here we study the dynamics of two competing pathogens in a structured host population and assess the impact of the mobility pattern of hosts on the pathogen competition. We model the spatial structure of the host population in terms of a metapopulation network and focus on two strains imported locally in the system and having the same transmission potential but different infectious periods. We find different scenarios leading to competitive success of either one of the strain or to the codominance of both strains in the system. The dominance of the strain characterized by the shorter or longer infectious period depends exclusively on the structure of the population and on the the mobility of hosts across patches. The proposed modeling framework allows the integration of other relevant epidemiological, environmental and demographic factors opening the path to further mathematical and computational studies of the dynamics of multipathogen systems.

q-bio.PE↗

arXiv2013

Age-specific contacts and travel patterns in the spatial spread of 2009 H1N1 influenza pandemic

Confirmed cases during the early stage of the 2009 H1N1 pdm in various countries showed an age shift between importations and local transmission cases, with adults mainly responsible for seeding unaffected regions and children most frequently driving community outbreaks. We introduce a multi-host stochastic metapopulation model with two age classes to analytically address the role of a heterogeneously mixing population and its associated non-homogeneous travel behaviors on the risk of a major epidemic. We inform the model with statistics on demography, mixing and travel behavior for Europe and Mexico, and calibrate it to the 2009 H1N1 pdm early outbreak. We varied model parameters to explore the invasion conditions under different scenarios. We derive the expression for the global invasion potential of the epidemic that depends on disease transmissibility, transportation network and mobility features, demographic profile and mixing pattern. Highly assortative mixing favor the spatial containment of the epidemic, this effect being contrasted by an increase in the social activity of adults vs. children. Heterogeneity of the mobility network topology and traffic flows strongly favor the disease invasion, as also a larger fraction of children traveling. Variations in the demography and mixing habits across countries lead to heterogeneous outbreak situations. Results are compatible with the H1N1 spatial spread observed. The work illustrates the importance of age-dependent mixing profiles and mobility features in the study of the conditions for the spatial invasion of an emerging influenza pandemic. Its results allow the immediate assessment of the risk of a major epidemic for a specific scenario upon availability of data, and the evaluation of the effectiveness of public health interventions targeting specific age groups, their interactions and mobility behaviors.

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arXiv2012

Heterogeneous length of stay of hosts' movements and spatial epidemic spread

Infectious diseases outbreaks are often characterized by a spatial component induced by hosts' distribution, mobility, and interactions. Spatial models that incorporate hosts' movements are being used to describe these processes, to investigate the conditions for propagation, and to predict the spatial spread. Several assumptions are being considered to model hosts' movements, ranging from permanent movements to daily commuting, where the time spent at destination is either infinite or assumes a homogeneous fixed value, respectively. Prompted by empirical evidence, here we introduce a general metapopulation approach to model the disease dynamics in a spatially structured population where the mobility process is characterized by a heterogeneous length of stay. We show that large fluctuations of the length of stay, as observed in reality, can have a significant impact on the threshold conditions for the global epidemic invasion, thus altering model predictions based on simple assumptions, and displaying important public health implications.

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arXiv2010

Modeling vaccination campaigns and the Fall/Winter 2009 activity of the new A(H1N1) influenza in the Northern Hemisphere

The unfolding of pandemic influenza A(H1N1) for Fall 2009 in the Northern Hemisphere is still uncertain. Plans for vaccination campaigns and vaccine trials are underway, with the first batches expected to be available early October. Several studies point to the possibility of an anticipated pandemic peak that could undermine the effectiveness of vaccination strategies. Here we use a structured global epidemic and mobility metapopulation model to assess the effectiveness of massive vaccination campaigns for the Fall/Winter 2009. Mitigation effects are explored depending on the interplay between the predicted pandemic evolution and the expected delivery of vaccines. The model is calibrated using recent estimates on the transmissibility of the new A(H1N1) influenza. Results show that if additional intervention strategies were not used to delay the time of pandemic peak, vaccination may not be able to considerably reduce the cumulative number of cases, even when the mass vaccination campaign is started as early as mid-October. Prioritized vaccination would be crucial in slowing down the pandemic evolution and reducing its burden.

q-bio.PE↗

arXiv2009

Seasonal transmission potential and activity peaks of the new influenza A(H1N1): a Monte Carlo likelihood analysis based on human mobility

On 11 June the World Health Organization officially raised the phase of pandemic alert (with regard to the new H1N1 influenza strain) to level 6. We use a global structured metapopulation model integrating mobility and transportation data worldwide in order to estimate the transmission potential and the relevant model parameters we used the data on the chronology of the 2009 novel influenza A(H1N1). The method is based on the maximum likelihood analysis of the arrival time distribution generated by the model in 12 countries seeded by Mexico by using 1M computationally simulated epidemics. An extended chronology including 93 countries worldwide seeded before 18 June was used to ascertain the seasonality effects. We found the best estimate R0 = 1.75 (95% CI 1.64 to 1.88) for the basic reproductive number. Correlation analysis allows the selection of the most probable seasonal behavior based on the observed pattern, leading to the identification of plausible scenarios for the future unfolding of the pandemic and the estimate of pandemic activity peaks in the different hemispheres. We provide estimates for the number of hospitalizations and the attack rate for the next wave as well as an extensive sensitivity analysis on the disease parameter values. We also studied the effect of systematic therapeutic use of antiviral drugs on the epidemic timeline. The analysis shows the potential for an early epidemic peak occurring in October/November in the Northern hemisphere, likely before large-scale vaccination campaigns could be carried out. We suggest that the planning of additional mitigation policies such as systematic antiviral treatments might be the key to delay the activity peak inorder to restore the effectiveness of the vaccination programs.

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