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Dances with worms: the ecological and evolutionary impacts of deworming on coinfecting pathogens. Parasitol 2013
"... Parasitic helminths are ubiquitous in most host, including human, populations. Helminths often alter the likelihood of infection and disease progression of coinfecting microparasitic pathogens (viruses, bacteria, protozoa), and there is great interest in incorporating deworming into control programm ..."
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Parasitic helminths are ubiquitous in most host, including human, populations. Helminths often alter the likelihood of infection and disease progression of coinfecting microparasitic pathogens (viruses, bacteria, protozoa), and there is great interest in incorporating deworming into control programmes for many major diseases (e.g. HIV, tuberculosis, malaria). However, such calls are controversial; studies show the consequences of deworming for the severity and spread of pathogens to be highly variable. Hence, the benefits of deworming, although clear for reducing themorbidity due to helminth infection per se, are unclear regarding the outcome of coinfections and comorbidities. I develop a theoretical framework to explore how helminth coinfection with other pathogens affects host mortality and pathogen spread and evolution under different interspecific parasite interactions. In all cases the outcomes of coinfection are highly context-dependent, depending on the mechanism of helminth-pathogen interaction and the quantitative level of helminth infection, with the effects of deworming potentially switching from beneficial to detrimental depending on helminth burden. Such context-dependency may explain some of the variation in the benefits of deworming seen between studies, and highlights the need for obtaining a quantitative understanding of parasite interactions across realistic helminth infection ranges. However, despite this complexity, this framework reveals predictable patterns in the effects of helminths that may aid the development of more effective, integrated management strategies to combat pathogens in this coinfected world.
Implications of vaccination and waning immunity
, 2011
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Evaluating the importance of within-and between-host selection pressures on the evolution of chronic pathogens
- Theor. Popul. Biol
, 2007
"... Abstract Infectious pathogens compete and are subject to natural selection at multiple levels. For example, viral strains compete for access to host resources within an infected host and, at the same time, compete for access to susceptible hosts within the host population. Here we propose a novel a ..."
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Abstract Infectious pathogens compete and are subject to natural selection at multiple levels. For example, viral strains compete for access to host resources within an infected host and, at the same time, compete for access to susceptible hosts within the host population. Here we propose a novel approach to study the interplay between within-and between-host competition. This approach allows for a single host to be infected by and transmit two strains of the same pathogen. We do this by nesting a model for the host-pathogen dynamics within each infected host into an epidemiological model. The nesting of models allows the between-host infectivity and mortality rates suffered by infected hosts to be functions of the disease progression at the within-host level. We present a general method for computing the basic reproduction ratio of a pathogen in such a model. We then illustrate our method using a basic model for the within-host dynamics of viral infections, embedded within the simplest susceptible-infected (SI) epidemiological model. Within this nested framework, we show that the virion production rate at the level of the cell-virus interaction leads, via within-host competition, to the presence or absence of between-host level competitive exclusion. In particular, we find that in the absence of mutation the strain that maximizes between-host fitness can outcompete all other strains. In the presence of mutation we observe a complex invasion landscape showing the possibility of coexistence. Although we emphasize the application to human viral diseases, we expect this methodology to be applicable to be many host-parasite systems. r
An epidemic model structured by host immunity
- Journal of Biological Systems
, 2006
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The role of host population heterogeneity in the evolution of virulence
- J Biol Dyn
"... I examine here the effects of host heterogeneity in the growth of immune response on the evolution and co-evolution of virulence. The analysis is based on an extension of the 'nested model' by Gilchrist and Sasaki [Modeling host-parasite coevolution, J. Theor. Biol. 218 Q1 assumptions is ..."
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I examine here the effects of host heterogeneity in the growth of immune response on the evolution and co-evolution of virulence. The analysis is based on an extension of the 'nested model' by Gilchrist and Sasaki [Modeling host-parasite coevolution, J. Theor. Biol. 218 Q1 assumptions is clarified why different results are present in the literature.
P. Agudelo-Romero and S. F. Elena* Instituto de Biología Molecular y Celular de Plantas (CSIC-UPV). Campus UPV CPI 8E.
"... The degree of plant resilience to infection correlates ..."
in viral respiratory tract infections
"... Note added March 2015: I have now written a shorter version of this paper, which I hope is argued better. It is available at ..."
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Note added March 2015: I have now written a shorter version of this paper, which I hope is argued better. It is available at
Research Interests Overview
"... I am interested in developing a quantitative understanding of the dynamics of pathogens and immune responses. The work of my group involves the use of mathematical models and computer simulations. We like nothing better than to validate models by confronting them with experimental data — we try to m ..."
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I am interested in developing a quantitative understanding of the dynamics of pathogens and immune responses. The work of my group involves the use of mathematical models and computer simulations. We like nothing better than to validate models by confronting them with experimental data — we try to make testable predictions, and in collaboration with experimentalists conduct the relevant experiments. We work in close collaboration with experimental immunologists, in particular the group of Dr. Rafi Ahmed at Emory. Our three main areas of investigation are: 1. The dynamics of infections and immune responses How do immune systems work? What determines whether an infection is short lived or chronic, and whether it generates lasting immunity? The answers to questions could help us design better vaccines, particularly towards persistent infections such as malaria and HIV. 2. Linking immunology and epidemiology Immunology and epidemiology are traditionally very different fields, yet they are intimately related. We have developed a theoretical framework to connect the withinhost dynamics of a pathogen with its transmission characteristics. We have used this framework to understand why pathogens harm their hosts, and under what conditions we expect a pathogens virulence to change. 3. The emergence, spread and evolution of infectious diseases How do pathogens emerge and spread through host populations? By addressing these general questions we can gain insight into the factors that have led to the emergence of HIV, SARS, and new strains of the influenza virus. This will allow us to predict what factors will be important in the emergence of infectious diseases in the future. My choice of one key publication in each of these three areas: 1. R. Antia, V. V. Ganusov, and R. Ahmed. The role of models in understanding CD8(+) T-cell memory. Nature Reviews Immunology, 5:101–11, 2005.
1 Pathogen competition and coexistence and the evolution of virulence
"... Summary. Competition between different strains of a micro-parasite which provide complete cross-protection and cross-immunity against each other selects for maximal basic replacement ratio if, in the absence of the disease, the host population is exclusively limited in its growth by a nonlinear popu ..."
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Summary. Competition between different strains of a micro-parasite which provide complete cross-protection and cross-immunity against each other selects for maximal basic replacement ratio if, in the absence of the disease, the host population is exclusively limited in its growth by a nonlinear population birth rate. For mass action incidence, the principle of R0 maximization can be extended to exponentially growing populations, if the exponential growth rate is small enough that the disease can limit population growth. For standard incidence, though not in full extent, it can be extended to populations which, without the disease, either grow exponentially or are growth-limited by a nonlinear population death rate, provided that disease prevalence is low and there is no immunity to the disease. If disease prevalence is high, strain competition rather selects for low disease fatality. A strain which would go extinct on its own can coexist with a more virulent strain by protecting from it, if it has strong vertical transmission. 1.1
Review TRENDS in Parasitology Vol.23 No.6 Transmission consequences of coinfection: cytokines writ large?
"... Coinfection of a host by multiple parasite species is commonly observed and recent epidemiological work indicates that coinfection can enhance parasite transmission. This article proposes an immunoepidemiological framework to understand how within-host interactions during coinfection might affect be ..."
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Coinfection of a host by multiple parasite species is commonly observed and recent epidemiological work indicates that coinfection can enhance parasite transmission. This article proposes an immunoepidemiological framework to understand how within-host interactions during coinfection might affect betweenhost transmission. Cytokines, immune signalling molecules with a fundamental role in the amplification of antiparasitic effector mechanisms, provide a useful way to simplify immunological complexity for this endeavour – focusing on cytokines offers analytical tractability without sacrificing realism. Testable predictions about the epidemiological consequences of coinfection are generated by this conceptual framework. Extrapolating from the individual to the population
