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PubMed2003

Challenging the trade-off model for the evolution of virulence: is virulence management feasible?

Progress in understanding the evolution of infectious diseases has inspired proposals to manage the evolution of pathogen (including parasite) virulence. A common view is that social interventions that lower pathogen transmission will indirectly select lower virulence because of a trade-off between transmission and virulence. Here, we argue that there is little theoretical justification and no empirical evidence for this plan. Although a trade-off model might apply to some pathogens, the mechanism appears too weak for rapid selection of substantial changes in virulence. Direct selection against virulence itself might be a more rewarding approach to managing the evolution of virulence.

Animals↗
PubMed1998

The evolution of virulence and emerging diseases.

Insights into the evolution of virulence may aid efforts to control or even prevent emerging diseases. Specifically, dangerous pathogens can be distinguished from those that pose relatively little threat by identifying characteristics that favor intense exploitation of hosts by pathogens, hence causing high virulence. Studies to date have implicated several such characteristics, including transmission by vectors, attendants, water, and durable propagules. These insights may improve the return on investments in disease control by directing effort and resources to the most-dangerous emerging pathogens. The approach also should help us to identify those control measures that will guard against the future emergence of dangerous pathogens, even those that have not yet been identified.

Arthropod Vectors↗
PubMed1998

Evolution of virulence: a unified framework for coinfection and superinfection.

Models of the evolution of parasite virulence have focused on computing the evolutionarily stable level of virulence favored by tradeoffs within a host and by competition for hosts, and deriving conditions under which strains with different virulence levels can coexist. The results depend on the type of interaction between disease strains, such as single infection (immunity of infected individuals to other strains), coinfection (simultaneous infection by two strains), and superinfection (instantaneous takeover of host by the more virulent strain). We present a coinfection model with two strains and derive the superinfection model as the limit where individuals are rapidly removed from the doubly-infectious class. When derived in this way, the superinfection model includes not only the takeover of hosts infected by the less virulent strain, but new terms which take into account the possibility of increased mortality of doubly-infected individuals. Coinfection tends to favor higher virulence and support more coexistence than the single infection model, but the detailed results depend sensitively on two factors: (1) whether and how the model is near the superinfection limit, and (2) the shape of the coinfection function (the function describing the rate at which a more virulent strain can infect a host). If the superinfection limit arises due to rapid mortality of doubly-infected hosts, there is a region of uninvadable virulence levels rather than coexistence. When the coinfection function is discontinuous, as in many previous models, neither the coinfection model nor the superinfection limit can support an evolutionarily stable virulence level. Piecewise differentiable and differentiable coinfection functions produce qualitatively different results, and we propose that these more general cases should be used to study evolution of virulence when other mechanisms like space, population dynamics, and stochasticity interact.

Animals↗
PubMed2002

Evolution and virulence of serogroup 6 pneumococci on a global scale.

To study the evolution and virulence of pneumococcal populations, we used multilocus sequence typing to identify the major clones among 212 carriage and invasive isolates expressing capsular serogroup 6 from 39 countries. The global population consisted of 8 major complexes and 6 minor complexes of related clones and 32 clones of diverse origin. Surprisingly, serotype 6A clones evolved by mutation nearly as often as by recombination, whereas serotype 6B clones evolved almost exclusively by recombination (P = 0.0029). This is the first report of population genetic differences among serotypes of this species. The largest clonal complex was associated with invasive disease (P = 0.019) and included a common ancestor for five previously identified drug-resistant clones. The putative ancestors of the major clonal complexes were represented by a greater proportion of carriage isolates than were their descendents (P = 0.001), and the ancestors tended to be less virulent than their descendents in a mouse model of infection. These data suggested that virulent serogroup 6 clones have evolved multiple times from less-virulent ancestral clones.

Adolescent↗
PubMed2000

Evolution of virulence in a heterogeneous host population.

There is a large body of theoretical studies that investigate factors that affect the evolution of virulence, that is parasite-induced host mortality. In these studies the host population is assumed to be genetically homogeneous. However, many parasites have a broad range of host types they infect, and trade-offs between the parasite virulence in different host types may exist. The aim of this paper is to study the effect of host heterogeneity on the evolution of parasite virulence. By analyzing a simple model that describes the replication of different parasite strains in a population of two different host types, we determine the optimal level of virulence in both host types and find the conditions under which strains that specialize in one host type dominate the parasite population. Furthermore, we show that intrahost evolution of the parasite during an infection may lead to stable polymorphisms and could introduce evolutionary branching in the parasite population.

Animals↗
PubMed2004

The evolution of virulence in pathogens with frequency-dependent transmission.

Frequency-dependent transmission is an important feature of diseases that are sexually transmitted or transmitted by a vector that actively searches for hosts. Here I describe the evolution of virulence in pathogens that have frequency-dependent transmission. I consider two components of virulence--an increase in host mortality due to infection, as is classically described, and a decrease in host fecundity due to infection, because frequency dependence is common among diseases that fully or partially sterilize their hosts. Theoretical predictions pertaining to host-pathogen numerical dynamics can be quite different between pathogens with frequency-dependent transmission and those with density-dependent transmission. In contrast, this study suggests that the principles governing the evolution of virulence that have been established in the context of density-dependent pathogens may also apply (qualitatively) to frequency-dependent pathogens. I examine the evolutionary trajectories of the mortality and sterility components of virulence as well as the role of spatial population structure in the evolution of the sterility component of virulence.

Animals↗
PubMed2002

Detection of the high-pathogenicity island of Yersinia enterocolitica in enterotoxigenic and enteropathogenic E.coli strains.

OBJECTIVE: To describe the distribution of high-pathogenicity island (HPI) of Yersinia enterocolitica in enterotoxingenic E.coli (ETEC) and enteropathogenic E.coli (EPEC), and to understand the structure and function of HPI. METHODS: PCR was used to detect irp2, fyua and asn-intB genes with subsequent sequence analysis of these genes. Nucleic acid in situ hybridization was employed to identify the specificity of irp2 and fyua. RESULTS: Thirty irp2-positive strains were isolated from 93 ETEC strains and 3 from 10 EPEC strains, making a positivity rate of 32.25% and 30% respectively, and the positivity rates of fyua gene in ETEC and EPEC were 21.51% and 30% respectively. In most of these positive isolates, HPI was bordered by an asn tRNA locus, as in Yersinia sp. CONCLUSIONS: This study demonstrates that the high positivity rate of HPI of Yersinia enterocolitica in ETEC and EPEC strains may be crucial to the virulence changes, virulence evolution and virulence regulation in E.coli.

Bacterial Outer Membrane Proteins↗
PubMed2002

Timing of transmission and the evolution of virulence of an insect virus.

We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts.

Analysis of Variance↗
PubMed1998

On the Relationship Between Evolution of Virulence and Host Demography.

The effects of density-dependence on the evolution of virulence in super-infection models is the theme of this paper. The qualitative dynamics of three host-pathogen systems are studied numerically in a virulence-superinfection parameter landscape. It is shown numerically that pathogen's competitive exclusion coexistence and host population extinction depend heavily of the population dynamics of the host population. Reported patterns of diversity found using models without demography, are insufficient to account for the coevolutionary dynamics under defined selective pressures. Specifically, virulence and superinfection in the presence of a variable host population give rise to threshold values that divide (as switches) the regions of coexistence and competitive exclusion. Tight coevolution on a variable host population may occur within regions of parameter space that are not connected. We present our numerical results using a simple host-disease system where a homogeneous host population is invaded by two competing pathogen strains (partial analytical results will be published elsewhere).Copyright 1998 Academic Press Limited

Journal Article↗
PubMed2025

Experimental evolution of a pathogen confronted with innate immune memory increases variation in virulence.

Understanding the drivers and mechanisms of virulence evolution is still a major goal of evolutionary biologists and epidemiologists. Theory predicts that the way virulence evolves depends on the balance between the benefits and costs it provides to pathogen fitness. Additionally, host responses to infections, such as resistance or tolerance, play a critical role in shaping virulence evolution. But, while the evolution of pathogens has been traditionally studied under the selection pressure of host adaptive immunity, less is known about their evolution when confronted to simpler and less effective forms of immunity such as immune priming. In this study, we used a well-established insect model for immune priming - red flour beetles and their bacterial pathogen Bacillus thuringiensis tenebrionis - to test how this form of innate immune memory drives the pathogen evolution. Through controlled experimental evolution of the pathogen in primed versus non-primed hosts, we found no change in average virulence after eight selection cycles in primed host. Nonetheless, we observed a notable rise in the variability of virulence, defined as the ability to kill hosts, among independent pathogen lines that evolved in primed hosts, and the bacteria were unable to develop resistance to host priming. Whole genome sequencing revealed increased activity in the bacterial mobilome (prophages and plasmids). Expression of the Cry toxin - a well-known virulence factor - was linked to evolved differences in copy number variation of the cry-carrying plasmid, though this did not correlate directly with virulence. These findings highlight that innate immune memory can drive variability in pathogen traits, which may favor adaptation to variable environments. This underscores the need to consider pathogen evolution in response to innate immune memory when applying these mechanisms in medicine, aquaculture, pest control, and insect mass production.

Animals↗
PubMed2004

The curse of the pharaoh in space: free-living infectious stages and the evolution of virulence in spatially explicit populations.

The idea that parasites with long-lived infective stages may evolve higher virulence has received considerable attention. This idea is called 'the curse of the pharaoh' because of the hypothesis that the death of Lord Carnavon was caused by very long-lived propagules of a highly virulent infectious disease. Here, we examined the evolution of diseases that transmit via free-living stages in a spatial context. We show that, if virulence evolves independently of transmission, long-lived infective stages can select for higher virulence. There is always the evolution of a finite transmission rate, which becomes higher when the infective stages are shorter lived. When a trade-off occurs between transmission and virulence, we show that there is no evidence for the curse of the pharaoh. Indeed, higher transmission and therefore virulence may be selected for by shorter rather than long-lived infective stages.

Animals↗
PubMed1999

Evolution of virulence factors in Shiga-toxin-producing Escherichia coli.

The major demonstrated or putative virulence factors of Shiga-toxin-producing Escherichia coli (STEC) are the Shiga toxins, products of the locus of enterocyte effacement, and products encoded by the EHEC-hemolysin plasmid. Molecular analysis shows that STEC acquired the majority of these virulence factors by horizontal transfer of genetic material. In the case of Shiga toxins, the phages encoding them are probably responsible for this transfer. For the locus of enterocyte effacement, however, it is not clear how often this transfer took place and which parts of the locus were involved in this transfer. The large EHEC-hemolysin plasmid is clearly a mosaic structure, which arose from multiple recombination events with foreign DNA. Two lineages of this plasmid can be distinguished, one of which is associated with chromosomally encoded virulence factors. Despite the wealth of information available, further comparative studies are needed to decipher definitively the evolution of virulence in STEC.

Escherichia coli↗
PubMed2006

Pathogen responses to host immunity: the impact of time delays and memory on the evolution of virulence.

Current analytical models of the mammalian immune system typically assume a specialist predator-prey relationship between invading pathogens and the active components of the immune response. However, in reality, the specific immune system is not immediately effective following invasion by a novel pathogen. First, there may be an explicit time delay between infection and immune initiation and, second, there may be a gradual build-up in immune efficacy (for instance, during the period of B-cell affinity maturation) during which the immune response develops, before reaching maximal specificity to the pathogen. Here, we use a novel theoretical approach to show that these processes, together with the presence of long-lived immune memory, decouple the immune response from current pathogen levels, greatly changing the dynamics of the pathogen-immune system interaction and the ability of the immune response to eliminate the pathogen. Furthermore, we use this model to show how distributed primary immune responses combine with immune memory to greatly affect the optimal virulence of the pathogen, potentially resulting in the evolution of highly virulent pathogens.

Animals↗
PubMed1995

The evolution of virulence in sexually transmitted HIV/AIDS.

A mathematical model is used to examine the effects of host population demography and transmission behavior on the evolution of virulence of a sexually transmitted pathogen such as HIV. The effect of the rate at which hosts acquire new partners is shown to depend critically on the details of the host population's growth pattern, sexual contact rate, and level of infection. At density-limited equilibrium, new partner acquisition rates have no effect on virulence. In an exponentially growing host population, higher partner acquisition rates favor the less virulent strain, as do lower rates of host population growth. In contrast, in uninfected populations, faster new partner acquisition rates encourage epidemics of the more virulent strain. Two extensions of the model--one including vertical transmission and another including within-host evolution--confirm the robustness of the predictions.

Acquired Immunodeficiency Syndrome↗
PubMed1995

[A modern view of the evolution of virulence].

According to the prevailing, traditional view parasites should develop reduced virulence towards their hosts, because more virulent pathogens are more likely to drive the hosts, and thus themselves to extinction. Virulence is considered to be a primitive stage of a parasitive-host association. However the usefulness and validity of this view have been questioned. Recent studies suggest that parasites need not necessarily evolve towards reduced virulence. The points of view of Darwinian medicine in the direction of the evolution of virulence there may be many possible coevolutionary trajectories, depending on the details of the parasite's life-history, the host's behavior and the transmissibility of the parasite. Theoretical and epidemiological evidences indicate that pathogens transmitted by arthropod vectors are significantly more lethal to humans than those transmitted by personal contact. Water borne enteric pathogens are less virulent after purification of water supplies. Recent experiments also support the emerging theory that parasitism can evolve to be either more or less virulent in a long-term host, depending on the way the parasite is transmitted to the host and on the environment in which they live.

Animals↗
PubMed2000

Parallel evolution of virulence in pathogenic Escherichia coli.

The mechanisms underlying the evolution and emergence of new bacterial pathogens are not well understood. To elucidate the evolution of pathogenic Escherichia coli strains, here we sequenced seven housekeeping genes to build a phylogenetic tree and trace the history of the acquisition of virulence genes. Compatibility analysis indicates that more than 70% of the informative sites agree with a single phylogeny, suggesting that recombination has not completely obscured the remnants of ancestral chromosomes. On the basis of the rate of synonymous substitution for E. coli and Salmonella enterica (4.7 x 10(-9) per site per year), the radiation of clones began about 9 million years ago and the highly virulent pathogen responsible for epidemics of food poisoning, E. coli O157:H7, separated from a common ancestor of E. coli K-12 as long as 4.5 million years ago. Phylogenetic analysis reveals that old lineages of E. coli have acquired the same virulence factors in parallel, including a pathogenicity island involved in intestinal adhesion, a plasmid-borne haemolysin, and phage-encoded Shiga toxins. Such parallel evolution indicates that natural selection has favoured an ordered acquisition of genes and the progressive build-up of molecular mechanisms that increase virulence.

DNA, Bacterial↗
PubMed1992

A kin selection model for the evolution of virulence.

The costs and benefits of parasite virulence are analysed in an evolutionarily stable strategy (ESS) model. Increased host mortality caused by disease (virulence) reduces a parasite's fitness by damaging its food supply. The fitness costs of high virulence may be offset by the benefits of increased transmission or ability to withstand the host's defences. It has been suggested that multiple infections lead to higher virulence because of competition among parasite strains within a host. A quantitative prediction is given for the ESS virulence rate as a function of the coefficient of relatedness among co-infecting strains. The prediction depends on the quantitative relation between the costs of virulence and the benefits of transmission or avoidance of host defences. The particular mechanisms by which parasites can increase their transmission or avoid host defences also have a key role in the evolution of virulence when there are multiple infections.

Animals↗