Multiple infections and the evolution of virulence

The discussion of host–parasite interactions, and of parasite virulence more specifically, has so far, with a few exceptions, not focused much attention on the accumulating evidence that immune evasion by parasites is not only almost universal but also often linked to pathogenesis, i.e. the appearance of virulence. Now, the immune evasion hypothesis offers a deeper insight into the evolution of virulence than previous hypotheses. Sensitivity analysis for parasite fitness and life-history theory shows promise to generate a more general evolutionary theory of virulence by including a major element, immune evasion to prevent parasite clearance from the host. Also, the study of dose–response relationships and multiple infections should be particularly illuminating to understand the evolution of virulence. Taking into account immune evasion brings immunological processes to the core of understanding the evolution of parasite virulence and for a range of related issues such as dose, host specificity or immunopathology. The aim of this review is to highlight the mechanism underlying immune evasion and to discuss possible consequences for the evolutionary ecology analysis of host–parasite interactions.

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Coevolution of virulence and immunosuppression in multiple infections

10.1101/149211 ◽

2017 ◽

Author(s):

Tsukushi Kamiya ◽

Nicole Mideo ◽

Samuel Alizon

Keyword(s):

Evolutionary Biology ◽

Adaptive Dynamics ◽

Multiple Infections ◽

Research Attention ◽

Background Mortality ◽

Evolution Of Virulence ◽

Duration Of Infection ◽

Peer Community ◽

The Cost ◽

Host Parasite

AbstractThis preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (http://dx.doi.org/10.24072/pci.evolbiol.100043). Many components of host-parasite interactions have been shown to affect the way virulence (i.e., parasite-induced harm to the host) evolves. However, coevolution of multiple parasite traits is often neglected. We explore how an immunosuppressive mechanism of parasites affects and coevolves with virulence through multiple infections. Applying the adaptive dynamics framework to epidemiological models with coinfection, we show that immunosuppression is a double-edged-sword for the evolution of virulence. On one hand, it amplifies the adaptive benefit of virulence by increasing the abundance of coinfections through epidemiological feedbacks. On the other hand, immunosuppression hinders host recovery, prolonging the duration of infection and elevating the cost of killing the host. The balance between the cost and benefit of immunosuppression varies across different background mortality rates of hosts. In addition, we find that immunosuppression evolution is influenced considerably by the precise trade-off shape determining the effect of immunosuppression on host recovery and susceptibility to further infection. These results demonstrate that the evolution of virulence is shaped by immunosuppression while highlighting that the evolution of immune evasion mechanisms deserves further research attention.

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Exposing the Diversity of Multiple Infection Patterns

10.1101/058263 ◽

2016 ◽

Author(s):

Mircea T. Sofonea ◽

Samuel Alizon ◽

Yannis Michalakis

Keyword(s):

Large Range ◽

Natural Populations ◽

Theoretical Models ◽

Multiple Infection ◽

Multiple Infections ◽

Ecological Interactions ◽

Chronic Infections ◽

Empirical Reality ◽

Evolution Of Virulence ◽

Host Infection

AbstractNatural populations often have to cope with genetically distinct parasites that can coexist, or not, within the same hosts. Theoretical models addressing the evolution of virulence have considered two within host infection outcomes, namely superinfection and coinfection. The field somehow became limited by this dichotomy that does not correspond to an empirical reality, as other infection patterns, namely sets of within-host infection outcomes, are possible. We indeed formally prove there are 114 different infection patterns for the sole recoverable chronic infections caused by horizontally-transmitted microparasites. We afterwards highlight eight infection patterns using an explicit modelling of within-host dynamics that captures a large range of ecological interactions, five of which have been neglected so far. To clarify the terminology related to multiple infections, we introduce terms describing these new relevant patterns and illustrate them with existing biological systems. This characterisation of infection patterns opens new perspectives for understanding the epidemiology and the evolution of parasites.

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Host sexual dimorphism affects the outcome of within-host pathogen competition

10.1101/306985 ◽

2018 ◽

Author(s):

Stephen A.Y. Gipson ◽

Luis Jimenez ◽

Matthew D. Hall

Keyword(s):

Competitive Ability ◽

Model System ◽

Multiple Infections ◽

Pasteuria Ramosa ◽

Host Sex ◽

Evolution Of Virulence ◽

Single Genotype ◽

Males And Females ◽

Multiple Pathogens ◽

Genotype Infection

AbstractNatural infections often consist multiple pathogens of the same or different species. In multiple infections, pathogens compete for access to host resources and fitness is determined by how well a pathogen can reproduce compared to its competitors. Given the propensity for males and females to exhibit variation in pathogen-induced reduction in lifespan or fecundity, we explore how host sex may modulate the competitive ability of pathogens, potentially favouring the transmission of different pathogen genotypes. Using the Daphnia magna - Pasteuria ramosa model system, we exposed male and female hosts to either a single genotype infection or coinfections consisting of two pathogen genotypes of varying levels of virulence, measured as pathogen-induced reduction in host lifespan. We found that co-infections within females generally favoured the transmission of the more virulent pathogen genotype. Conversely, co-infections within male hosts resulted in equal transmission of competing genotypes, or favoured the transmission of the less virulent pathogen genotype in treatments where it established prior to the more virulent competitor. These results suggest that sex is a form of host heterogeneity which may influence the evolution of virulence within co-infection contexts and that one sex may be a reservoir for pathogen genetic diversity in nature.

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THE EFFECTS OF MULTIPLE INFECTIONS ON THE EXPRESSION AND EVOLUTION OF VIRULENCE IN ADAPHNIA-ENDOPARASITE SYSTEM

Evolution ◽

10.1111/j.1558-5646.2008.00391.x ◽

2008 ◽

Vol 62 (7) ◽

pp. 1700-1711 ◽

Cited By ~ 89

Author(s):

Frida Ben-Ami ◽

Laurence Mouton ◽

Dieter Ebert

Keyword(s):

Multiple Infections ◽

Evolution Of Virulence

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From within-host interactions to epidemiological competition: a general model for multiple infections

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2014.0303 ◽

2015 ◽

Vol 370 (1675) ◽

pp. 20140303 ◽

Cited By ~ 25

Author(s):

Mircea T. Sofonea ◽

Samuel Alizon ◽

Yannis Michalakis

Keyword(s):

Analytical Solutions ◽

General Model ◽

Population Level ◽

Host Population ◽

Multiple Infections ◽

Transmission Network ◽

Host Interactions ◽

Transmission Rates ◽

Evolution Of Virulence ◽

Host Growth

Many hosts are infected by several parasite genotypes at a time. In these co-infected hosts, parasites can interact in various ways thus creating diverse within-host dynamics, making it difficult to predict the expression and the evolution of virulence. Moreover, multiple infections generate a combinatorial diversity of cotransmission routes at the host population level, which complicates the epidemiology and may lead to non-trivial outcomes. We introduce a new model for multiple infections, which allows any number of parasite genotypes to infect hosts and potentially coexist in the population. In our model, parasites affect one another's within-host growth through density-dependent interactions and by means of public goods and spite. These within-host interactions determine virulence, recovery and transmission rates, which are then integrated in a transmission network. We use analytical solutions and numerical simulations to investigate epidemiological feedbacks in host populations infected by several parasite genotypes. Finally, we discuss general perspectives on multiple infections.

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