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PubMed2005

Evolution of virulence: interdependence, constraints, and selection using nested models.

Natural selection acts on virus populations at two distinct but interrelated levels: within individual hosts and between them. Studies of the evolution of virulence typically focus on selection acting at the epidemiological or between-host level and demonstrate the importance of trade-offs between disease transmission and virulence rates. Within-host studies reach similar conclusions regarding trade-offs between transmission and virulence at the level of individual cells. Studies which examine selection at both scales assume that between- and within-host selection are necessarily in conflict. We explicitly examine these ideas and assumptions using a model of within-host viral dynamics nested within a model of between-host disease dynamics. Our approach allows us to evaluate the direction of selection at the within- and between-host levels and identify situations leading to conflict and accord between the two levels of selection.

Host-Parasite Interactions↗
PubMed1991

Waterborne transmission and the evolution of virulence among gastrointestinal bacteria.

Diarrhoeal diseases are primary contributors to millions of deaths annually. Yet, little is known about the evolutionary reasons for the differences in virulence among gastrointestinal pathogens. Applying the comparative, cost/benefit approach of evolutionary biology this paper proposes that waterborne transmission should favour evolution towards high virulence. This hypothesis is supported by a cross-specific test, which shows that waterborne transmission is strongly correlated with the virulence of bacterial gastrointestinal pathogens of humans. Alternative explanations of this correlation are not supported by available data. These findings bear on public health policy because they draw attention to a previously unrecognized long-range benefit gained from purification of water supplies; diarrhoeal pathogens may evolve to lower levels of virulence.

Bacteria↗
PubMed2004

Complete genomes of two clinical Staphylococcus aureus strains: evidence for the rapid evolution of virulence and drug resistance.

Staphylococcus aureus is an important nosocomial and community-acquired pathogen. Its genetic plasticity has facilitated the evolution of many virulent and drug-resistant strains, presenting a major and constantly changing clinical challenge. We sequenced the approximately 2.8-Mbp genomes of two disease-causing S. aureus strains isolated from distinct clinical settings: a recent hospital-acquired representative of the epidemic methicillin-resistant S. aureus EMRSA-16 clone (MRSA252), a clinically important and globally prevalent lineage; and a representative of an invasive community-acquired methicillin-susceptible S. aureus clone (MSSA476). A comparative-genomics approach was used to explore the mechanisms of evolution of clinically important S. aureus genomes and to identify regions affecting virulence and drug resistance. The genome sequences of MRSA252 and MSSA476 have a well conserved core region but differ markedly in their accessory genetic elements. MRSA252 is the most genetically diverse S. aureus strain sequenced to date: approximately 6% of the genome is novel compared with other published genomes, and it contains several unique genetic elements. MSSA476 is methicillin-susceptible, but it contains a novel Staphylococcal chromosomal cassette (SCC) mec-like element (designated SCC(476)), which is integrated at the same site on the chromosome as SCCmec elements in MRSA strains but encodes a putative fusidic acid resistance protein. The crucial role that accessory elements play in the rapid evolution of S. aureus is clearly illustrated by comparing the MSSA476 genome with that of an extremely closely related MRSA community-acquired strain; the differential distribution of large mobile elements carrying virulence and drug-resistance determinants may be responsible for the clinically important phenotypic differences in these strains.

Drug Resistance, Bacterial↗
PubMed2003

Trade-offs and the evolution of virulence of microparasites: do details matter?

Models of the within-host dynamics of parasites have been used to consider the evolution of microparasites causing acute infections in vertebrate hosts. In this paper, we use these models to examine how the level of virulence to which a parasite evolves, depends on factors such as the relationship between parasite density and its rate of transmission from infected hosts, and the mechanism of parasite-induced pathogenesis. We show that changes in the terms describing transmissibility and pathogenesis may lead to dramatic differences in the level of virulence to which a parasite evolves. This suggests that no single factor is likely to be responsible for the differences in virulence of different parasites, and that understanding of the evolution of virulence of parasites will require a detailed quantitative understanding of the interaction between the parasite and its host.

Adaptation, Biological↗
PubMed2005

Intraspecific competition and the evolution of virulence in a parasitic trematode.

Intrahost competition between parasite genotypes has been predicted to be an important force shaping parasite ecology and evolution and has been extensively cited as a mechanism for the evolution of increased parasite virulence. However, empirical evidence demonstrating the existence and nature of intraspecific competition is lacking for many parasites. Here, we compared within-host competitiveness between genetic strains of Schistosoma mansoni with high (HIGH-V) or low (LOW-V) virulence to their intermediate snail host, Biomphalaria glabrata. Groups of snails were exposed to either one or the other of two parasite strains, or a mixed infection of both strains, and the resulting progeny were identified using a molecular marker. In two separate experiments investigating simultaneous and sequential infections, we demonstrated that the lifetime reproductive success of parasite strain HIGH-V was reduced in the presence of a faster replicating parasite genotype, LOW-V, regardless of whether it was in a majority or minority in the initial inoculum of the simultaneous exposure or of its relative position in the sequential exposure experiment. Thus, we demonstrate competition between parasite genotypes and asymmetry in competitive success between parasite strains. Moreover, since the less virulent strain investigated here had a competitive advantage, we suggest that a high frequency of multiple infections could favor the evolution of less, rather than more, virulent parasites in this system.

Animals↗
PubMed1990

Selection and evolution of virulence in bacteria: an ecumenical excursion and modest suggestion.

Why do parasites kill their hosts? During this past decade, research in three different areas; evolutionary ecology, medical microbiology, and population genetics has provided theory and data that address this and related questions of selection and the evolution and maintenance of parasite virulence. A general theory of parasite-host coevolution and the conditions for selection to favour parasite virulence has been put forth. Considerable advances have been made in elucidating the mechanisms of pathogenicity and inheritance of virulence in bacteria. The population genetic structure and the relationship between pathogenic and non-pathogenic forms has been determined for a number of species of bacteria. We critically review these developments and their implications for questions of selection and the evolution and maintenance of virulence in bacteria. We postulate how selection may operate on specific types of bacterial virulence and present a general protocol to experimentally test hypotheses concerning selection and the evolution of virulence in bacteria.

Animals↗
PubMed1998

The effect of different immune responses on the evolution of virulent CXCR4-tropic HIV.

We use mathematical models to determine possible mechanisms contributing to the evolution and rise of virulent CXCR4-tropic HIV in vivo. The models predict that the ability of the virus to specialize on a given target cell type depends on the exact fitness landscape of the viral mutants. Because this fitness landscape varies between people, this may explain why the evolution of fully CXCR4-tropic strains only occurs in about 50% of infected patients. Assuming that CXCR4-tropic HIV may evolve, we investigate the effect of different immune responses on the rise of such virulent strains. If we assume that CXCR4-tropic HIV is more cytopathic than CCR5-tropic virus, virulent CXCR4-tropic mutants remain suppressed at low levels both in the absence of an immune response, and in the presence of responses that act on the virus before integration into the host genome. On the other hand, this difference in cytopathogenicity is reduced by the presence of immune responses acting on infected cells, allowing CXCR4-tropic HIV to coexist with the CCR5-tropic virus. These results may help to interpret experimental data and are discussed with reference to the literature.

HIV↗
PubMed2001

Trade-offs in the evolution of virulence in an indirectly transmitted macroparasite.

The adaptive trade-off theory for the evolution and maintenance of parasite virulence requires that virulence be genetically correlated with other fitness characteristics of the parasite. Many theoretical models rely on a positive correlation between virulence and transmissibility. They assume that high parasite replication rates are associated with a high probability of transmission (and, hence, increased parasite fitness), but also with high levels of damage to the host (high virulence). Schistosomes are macroparasites with an indirect life cycle involving a mammalian and a molluscan host. Here we demonstrate, through the development of five substrains, a genetic basis for schistosome virulence. We used these substrains further in order to investigate the presence of parasite fitness traits that were genetically correlated with virulence. High virulence in the (mouse) definitive host was, as predicted, positively correlated with parasite replication. In contrast, in the (snail) intermediate host high virulence was associated with low parasite replication rates. Variation in infectivity to and parasite replication in the definitive host was suggested as a compensating mechanism for the maintenance of virulence in the snail host. This is the first report of a trade-off in parasite reproductive success across hosts in an indirectly transmitted macroparasite.

Adaptation, Physiological↗
PubMed2005

Evolution of virulence: coinfection and propagule production in spore-producing parasites.

BACKGROUND: The evolution of within-host growth rates by parasites is expected to depend on a trade-off between propagule production and virulence. The presence of coinfections, however, is thought to alter this trade-off, and hence alter the evolutionarily stable strategy (ESS) for the parasite. Here I consider a model wherein the number of coinfections that are identical by descent can depend on the parasite's reproductive strategy. Transmission success was treated as being either a negative-linear or a negative-exponential function of the total number of propagules produced by all coinfections. RESULTS: Increasing the number of unrelated coinfections either selected for a decrease in reproductive output by the parasite (linear case), or had no effect on the ESS (exponential case). Nonetheless, the total number of propagules produced within each host increased in both cases. Increasing the relatedness among coinfections, however, selected for reductions in parasite reproduction in both cases. CONCLUSION: Unrelated coinfection may increase overall parasite virulence, but the result stems from adding more infections rather than to more aggressive growth by the individual infections. However, all else being equal, if the coinfections are more related than expected by chance alone, then the total reproductive output by all coinfections would be expected to be reduced, resulting in reduced virulence.

Adaptation, Biological↗
PubMed2004

The evolution of virulence when parasites cause host castration and gigantism.

It has been suggested that the harm parasites cause to their hosts is an unavoidable consequence of parasite reproduction with costs not only for the host but also for the parasite. Castrating parasites are thought to minimize their costs by reducing host fecundity, which may minimize the chances of killing both host and parasite prematurely. We conducted a series of experiments to understand the evolution of virulence of a castrating bacterium in the planktonic crustacean Daphnia magna. By manipulating food levels during the infection of D. magna with the bacterium Pasteuria ramosa, we showed that both antagonists are resource-limited and that a negative correlation between host and parasite reproduction exists, indicating resource competition among the antagonists. Pasteuria ramosa also induces enhanced growth of its hosts (gigantism), which we found to be negatively correlated with host fecundity but positively correlated with parasite reproduction. Because infected hosts never recovered from infections, we concluded that gigantism is beneficial only for the parasite. Hosts, however, have evolved counteradaptations. We showed that infected hosts have enhanced reproduction before castration. This shift to earlier reproduction increases overall host fecundity and compromises parasite reproduction. Finally, we showed that this resource conflict is subject to genetic variation among host and parasite genotypes within a population and is therefore likely to be an important force in the coevolution of virulence in this system. A verbal model is presented and suggests that the adaptive value of gigantism is to store host resources, which are liberated after parasitic castration for later use by the growing parasite. This hypothesis assumes that infections are long lasting, that is, that they have a high life expectancy.

Adaptation, Physiological↗
PubMed1999

Population dynamics and the evolution of virulence in epidemiological models with discrete host generations

Chaos is the likely outcome of the interaction between a parasite and a host with discrete generations, if the parasite's virulence is high and if transmission from one generation to the next is held constant. We studied two alternative routes of transmission-vertical transmission from infecteds to their offspring, and transmission via long-lasting spores produced in those individuals that were killed by the infection-to investigate the influence of the transmission route on the system's evolution and population dynamics. The major results are: (1) vertical transmission often leads to low virulence, thus confirming most epidemiological models. However, if hosts can become super-infected, the evolutionary dynamics of virulence can have several equilibrium points, including 100% disease-induced mortality; (2) when parasites are transmitted with long-lasting spores, the evolutionary dynamics of virulence can become unstable, leading to the repeated bifurcation of two sub-populations with high and low virulence or to punctuated equilibria with sudden changes in the average level of virulence; (3) in general, the evolution of virulence moves the system to an area where the population dynamics are stable. When evolution leads to chaos, the system most often becomes extinct. Only for a restricted parameter space in the system where transmission from one generation to the next is via long-lasting spores do the dynamics become chaotic without extinction of the system. Copyright 1999 Academic Press.

Journal Article↗
PubMed1994

The evolution of virulence in parasites and pathogens: reconciliation between two competing hypotheses.

According to conventional wisdom, parasites and pathogens should evolve reduced virulence to their hosts, because more virulent parasites and pathogens are more likely to drive their hosts, and themselves, to extinction. But this view has been criticized for its reliance on group selection. According to an alternative perspective, selection will favor whatever level of virulence maximizes the rate of increase of the parasite or pathogen. This optimum virulence depends on the functional relationship between a parasite or pathogen's transmissibility and its effect on host mortality, with selection often favoring an intermediate degree of virulence. The thesis of this paper is that models in which intermediate levels of virulence are favored lead quite naturally to the further conclusion that parasites and pathogens should-up to a point-become less virulent over time, once the feedbacks between ecological and evolutionary processes are incorporated into the analysis. As a consequence of successive adaptations by the parasite or pathogen, the density of susceptible hosts is reduced, thereby altering the balance between selective forces so as to favor reduced virulence. However, the evolutionarily stable strategy that is achieved is bounded away from complete avirulence. We conclude that models in which intermediate virulence is favored do not necessarily contradict the conventional wisdom in the long run; in fact, these models provide a simple mechanistic explanation for the evolution of reduced virulence.

Animals↗
PubMed2005

Insights on evolution of virulence and resistance from the complete genome analysis of an early methicillin-resistant Staphylococcus aureus strain and a biofilm-producing methicillin-resistant Staphylococcus epidermidis strain.

Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. Staphylococcus epidermidis has emerged as a causative agent of infections often associated with implanted medical devices. We have sequenced the approximately 2.8-Mb genome of S. aureus COL, an early methicillin-resistant isolate, and the approximately 2.6-Mb genome of S. epidermidis RP62a, a methicillin-resistant biofilm isolate. Comparative analysis of these and other staphylococcal genomes was used to explore the evolution of virulence and resistance between these two species. The S. aureus and S. epidermidis genomes are syntenic throughout their lengths and share a core set of 1,681 open reading frames. Genome islands in nonsyntenic regions are the primary source of variations in pathogenicity and resistance. Gene transfer between staphylococci and low-GC-content gram-positive bacteria appears to have shaped their virulence and resistance profiles. Integrated plasmids in S. epidermidis carry genes encoding resistance to cadmium and species-specific LPXTG surface proteins. A novel genome island encodes multiple phenol-soluble modulins, a potential S. epidermidis virulence factor. S. epidermidis contains the cap operon, encoding the polyglutamate capsule, a major virulence factor in Bacillus anthracis. Additional phenotypic differences are likely the result of single nucleotide polymorphisms, which are most numerous in cell envelope proteins. Overall differences in pathogenicity can be attributed to genome islands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S. epidermidis.

Biofilms↗
PubMed1994

The evolution of virulence.

Why is there variation in the virulence of infectious diseases? Virulence can have substantial effects on the genetic contribution of both host and pathogen to future generations. Understanding it therefore requires explanation not only in terms of cellular and molecular mechanisms, but also in evolutionary terms: what is the nature of the selection acting on genes responsible for virulence?

Animals↗
PubMed1999

'Small worlds' and the evolution of virulence: infection occurs locally and at a distance.

Why are some discases more virulent than others? Vector-borne diseases such as malaria and water-borne diseases such as cholera are generally more virulent than diseases spread by direct contagion. One factor that characterizes both vector- and water-borne diseases is their ability to spread over long distances, thus causing infection of susceptible individuals distant from the infected individual. Here we show that this ability of the pathogen to infect distant individuals in a spatially structured host population leads to the evolution of a more virulent pathogen. We use a lattice model in which reproduction is local but infection can vary between completely local to completely global. With completely global infection the evolutionarily stable strategy (ESS) is the same as in mean-field models while a lower virulence is predicted as infection becomes more local. There is characteristically a period of relatively moderate increase in virulence followed by a more rapid rise with increasing proportions of global infection as we move beyond a 'critical connectivity'. In the light of recent work emphasizing the existence of 'small world' networks in human populations, our results suggests that if the world is getting 'smaller'--as populations become more connected--diseases may evolve higher virulence.

Animals↗
PubMed2000

Molecular evolution of virulence in natural field strains of Xanthomonas campestris pv. vesicatoria.

The avrBs2 avirulence gene of the bacterial plant pathogen Xanthomonas campestris pv. vesicatoria triggers disease resistance in pepper plants containing the Bs2 resistance gene and contributes to bacterial virulence on susceptible host plants. We studied the effects of the pepper Bs2 gene on the evolution of avrBs2 by characterizing the molecular basis for virulence of 20 X. campestris pv. vesicatoria field strains that were isolated from disease spots on previously resistant Bs2 pepper plants. All field strains tested were complemented by a wild-type copy of avrBs2 in their ability to trigger disease resistance on Bs2 plants. DNA sequencing revealed four mutant alleles of avrBs2, two of which consisted of insertions or deletions of 5 nucleotides in a repetitive region of avrBs2. The other two avrBs2 alleles were characterized by point mutations with resulting single amino acid changes (R403P or A410D). We generated isogenic X. campestris pv. vesicatoria strains by chromosomal avrBs2 gene exchange to study the effects of these mutations on the dual functions of avrBs2 in enhancing bacterial virulence and inducing plant resistance by in planta bacterial growth experiments. The deletion of 5 nucleotides led to loss of avrBs2-induced resistance on Bs2 pepper plants and abolition of avrBs2-mediated enhancement of fitness on susceptible plants. Significantly, the point mutations led to minimal reduction in virulence function of avrBs2 on susceptible pepper plants, with either minimal (R403P allele) or an intermediate level of (A410D allele) triggering of resistance on Bs2 plants. Consistent with the divergent selection pressures on avrBs2 exerted by the Bs2 resistance gene, our results show that avrBs2 is evolving to decrease detection by the Bs2 gene while at the same time maintaining its virulence function.

Amino Acid Sequence↗