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PubMed2004

Evolution of virulence.

At the close of the 19th century, the germ theory had generated a new understanding of the causes of acute infectious diseases and revealed new directions for study. This understanding contributed to the greatest improvements in health in the history of medicine. At the end of the 20th century, the second stage of this disciplinary development is occurring. The old germ theory is being expanded into a new germ theory, which, by integrated the full spectrum of biologic disciplines. This new germ theory is emphasizing how environments and human activities influence the characteristics of infectious agents and the broader role of infection as a cause of chronic diseases.

Animals↗
PubMed2004

[Evolution and virulence of primate lentiviruses].

While the AIDS epidemic caused by human immunodeficiency viruses (HIV) has resulted in the death of over 20 million people worldwide, simian immunodeficiency virus (SIV) infection, found in numerous African primate species, does not induce disease symptoms. The factors accounting for this difference between humans and natural host of SIV remain poorly understood. The entangled nature of the host/virus relationship could be the answer, rather than independent virus or host factors. Such a relationship is as a consequence of host/virus adaptation which has evolved over long periods in naturally infected primate species.

Adaptation, Physiological↗
PubMed2002

Candida commensalism and virulence: the evolution of phenotypic plasticity.

Candida albicans and related species live as benign commensals in one or more body locations in a majority of healthy individuals. As opportunistic pathogens, they are poised to overgrow cavities and penetrate tissue in response to an alteration in host physiology that presumably compromises the immune functions that normally suppress their growth. There is little evidence of the emergence of successful drug-resistant or hypervirulent strains that predominate in either the commensal or disease states. It appears more likely that all strains possess similar capabilities for rapid adaptation to drug therapy, the immune response and changes in body location and in host physiology. It is suggested that the mechanisms for rapid adaptation lie in the developmental programs of the bud-hypha transition and high frequency phenotypic switching, and in the modulation of the expression of virulence genes in response to environmental cues.

Adult↗
PubMed2001

Evolution of pathogen virulence: the role of variation in host phenotype.

Selection on pathogens tends to favour the evolution of growth and reproductive rates and a concomitant level of virulence (damage done to the host) that maximizes pathogen fitness. Yet, because hosts often pose varying selective environments to pathogens, one level of virulence may not be appropriate for all host types. Indeed, if a level of virulence confers high fitness to the pathogen in one host phenotype but low fitness in another host phenotype, alternative virulence strategies may be maintained in the pathogen population. Such strategies can occur either as polymorphism, where different strains of pathogen evolve specialized virulence strategies in different host phenotypes or as polyphenism, where pathogens facultatively express alternative virulence strategies depending on host phenotype. Polymorphism potentially leads to specialist pathogens capable of infecting a limited range of host phenotypes, whereas polyphenism potentially leads to generalist pathogens capable of infecting a wider range of hosts. Evaluating how variation among hosts affects virulence evolution can provide insight into pathogen diversity and is critical in determining how host pathogen interactions affect the phenotypic evolution of both hosts and pathogens.

Biological Evolution↗
PubMed1994

Kin selection and virulence in the evolution of protocells and parasites.

The evolution of parasite virulence and the origin of cooperative genomes in primitive cells are both problems that balance cooperative and competitive interactions among symbionts. I analyse the trade-off among three correlated traits: competitiveness against other genotypes for resources within hosts (protocells), damage to the host (virulence), and rate of horizontal transmission from one host to another. All three life-history components are strongly influenced by kin selection. For example, when genetic relatedness within hosts is high, each genotype is competing for resources with closely related genotypes. This competition among relatives favours increased horizontal transmission to colonize new hosts and compete against non-relatives. My analysis shows that many aspects of parasite and protocell evolution must be studied with the theoretical tools of social evolution. I discuss extensions that are required for a general theory of symbiosis.

Animals↗
PubMed2003

[Study on the prevalence of the "high pathogenicity island" of Yersinia enterocolitica WA in Enterotoxigenic, Enteropathogenic and Enteroaggregative E. coli strains].

OBJECTIVE: To detect the "high pathogenicity island" of Yersinia enterocolitica WA in E. coli and the to provide evidence for theory base of bacterial evolution process and the different structures in different E. coil. METHODS: Polymerase chain reaction (PCR), nucleic acid hybridization in situ were used to detect and identify HPI. DNA sequencing was used to compare the gene homology of HPI among E. coli with Yersinia enterocolitica (Yen). RESULTS: The irp2 and fyua genes of Yen HPI were investigated in E. coli strains. Among them, 30 strains were isolated from 93 Enterotoxigenic E. coli (ETEC) strains and 3 strains were positive in 10 strains Enteropathogenic (EPEC). HPI was also detected in Enteroaggregative E. coli (EAggEC) strain. In most of these isolates, HPI was bordered by an asntRNA locus, as in Yersinia sp. Through sequential comparison, the gene sequence homology was higher between in EPEC and EAggEC than ETEC and Yersinia enterocolica. CONCLUSIONS: ETEC, EPEC and EAggEC were pathogenicity bacterias and many of them harboring HPI of Yen and the HPI had the same position in E. coli chromosome as Yersinia enterocolitica but the diversity of structure and sequence in these E. coli might suggest that the HPI of these different serotype E. coli were from different ancient bacterias. At the same time, the high positivity rate of HPI in E. coli might be crucial to virulence change, virulence evolution and virulence regulation in E. coli.

Bacterial Proteins↗
PubMed1999

The agricultural pathology of ant fungus gardens.

Gardens of fungus-growing ants (Formicidae: Attini) traditionally have been thought to be free of microbial parasites, with the fungal mutualist maintained in nearly pure "monocultures." We conducted extensive isolations of "alien" (nonmutualistic) fungi from ant gardens of a phylogenetically representative collection of attine ants. Contrary to the long-standing assumption that gardens are maintained free of microbial pathogens and parasites, they are in fact host to specialized parasites that are only known from attine gardens and that are found in most attine nests. These specialized garden parasites, belonging to the microfungus genus Escovopsis (Ascomycota: anamorphic Hypocreales), are horizontally transmitted between colonies. Consistent with theory of virulence evolution under this mode of pathogen transmission, Escovopsis is highly virulent and has the potential for rapid devastation of ant gardens, leading to colony mortality. The specialized parasite Escovopsis is more prevalent in gardens of the more derived ant lineages than in gardens of the more "primitive" (basal) ant lineages. Because fungal cultivars of derived attine lineages are asexual clones of apparently ancient origin whereas cultivars of primitive ant lineages were domesticated relatively recently from free-living sexual stocks, the increased virulence of pathogens associated with ancient asexual cultivars suggests an evolutionary cost to cultivar clonality, perhaps resulting from slower evolutionary rates of cultivars in the coevolutionary race with their pathogens.

Journal Article↗
PubMed2002

Does multiple infection select for raised virulence?

Classical models of virulence evolution conclude that the increased competition favoured by multiple infection will select for increasing consumption and deterioration of the host resource, or 'virulence'. However, recent empirical and theoretical studies suggest that this view of virulence has some shortcomings. Here, we argue that the evolutionary consequences of multiple infection depend critically on whether the exploitation rate of an individual parasite is governed directly by the behaviour of the individual, or whether it is limited by the collective behaviour of the coinfecting group. We illustrate that, depending on the mechanistic details of exploitation, multiple infection can select for reduced virulence.

Biological Evolution↗
PubMed2001

Imperfect vaccines and the evolution of pathogen virulence.

Vaccines rarely provide full protection from disease. Nevertheless, partially effective (imperfect) vaccines may be used to protect both individuals and whole populations. We studied the potential impact of different types of imperfect vaccines on the evolution of pathogen virulence (induced host mortality) and the consequences for public health. Here we show that vaccines designed to reduce pathogen growth rate and/or toxicity diminish selection against virulent pathogens. The subsequent evolution leads to higher levels of intrinsic virulence and hence to more severe disease in unvaccinated individuals. This evolution can erode any population-wide benefits such that overall mortality rates are unaffected, or even increase, with the level of vaccination coverage. In contrast, infection-blocking vaccines induce no such effects, and can even select for lower virulence. These findings have policy implications for the development and use of vaccines that are not expected to provide full immunity, such as candidate vaccines for malaria.

Adaptation, Physiological↗
PubMed2001

Host life history and the evolution of parasite virulence.

We present a general epidemiological model of host-parasite interactions that includes various forms of superinfection. We use this model to study the effects of different host life-history traits on the evolution of parasite virulence. In particular, we analyze the effects of natural host death rate on the evolutionarily stable parasite virulence. We show that, contrary to classical predictions, an increase in the natural host death rate may select for lower parasite virulence if some form of superinfection occurs. This result is in agreement with the experimental results and the verbal argument presented by Ebert and Mangin (1997). This experiment is discussed in the light of the present model. We also point out the importance of superinfections for the effect of nonspecific immunity on the evolution of virulence. In a broader perspective, this model demonstrates that the occurrence of multiple infections may qualitatively alter classical predictions concerning the effects of various host life-history traits on the evolution of parasite virulence.

Animals↗
PubMed2006

Pervasive purifying selection characterizes the evolution of I2 homologs.

We sampled 384 sequences related to the Solanum pimpinellifolium (=Lycopersicon pimpinellifolium) disease resistance (R) gene 12 from six species, potato, S. demissum, tomato, eggplant, pepper, and tobacco. These species represent increasing phylogenetic distance from potato to tobacco, within the family Solanaceae. Using sequence data from the nucleotide binding site (NBS) region of this gene, we tested models of gene family evolution and inferred patterns of selection acting on the NBS gene region and I2 gene family. We find that the I2 family has diversified within the family Solanaceae for at least 14 million years and evolves through a slow birth-and-death process requiring approximately 12 million years to homogenize gene copies within a species. Analyses of selection resolved a general pattern of strong purifying selection acting on individual codon positions within the NBS and on NBS lineages through time. Surprisingly, we find nine codon positions strongly affected by positive selection and six pairs of codon positions demonstrating correlated amino acid substitutions. Evolutionary analyses serve as bioinformatic tools with which to sort through the vast R gene diversity in plants and find candidates for new resistance specificities or to identify specific amino acid positions important for biochemical function. The slow birth-and-death evolution of I2 genes suggests that some NBS-leucine rich repeat-mediated resistances may not be overcome rapidly by virulence evolution and that the natural diversity of R genes is a potentially valuable source for durable resistance.

DNA-Binding Proteins↗
PubMed2004

Experimental evaluation of the relationship between lethal or non-lethal virulence and transmission success in malaria parasite infections.

BACKGROUND: Evolutionary theory suggests that the selection pressure on parasites to maximize their transmission determines their optimal host exploitation strategies and thus their virulence. Establishing the adaptive basis to parasite life history traits has important consequences for predicting parasite responses to public health interventions. In this study we examine the extent to which malaria parasites conform to the predicted adaptive trade-off between transmission and virulence, as defined by mortality. The majority of natural infections, however, result in sub-lethal virulent effects (e.g. anaemia) and are often composed of many strains. Both sub-lethal effects and pathogen population structure have been theoretically shown to have important consequences for virulence evolution. Thus, we additionally examine the relationship between anaemia and transmission in single and mixed clone infections. RESULTS: Whereas there was a trade-off between transmission success and virulence as defined by host mortality, contradictory clone-specific patterns occurred when defining virulence by anaemia. A negative relationship between anaemia and transmission success was found for one of the parasite clones, whereas there was no relationship for the other. Notably the two parasite clones also differed in a transmission phenotype (gametocyte sex ratio) that has previously been shown to respond adaptively to a changing blood environment. In addition, as predicted by evolutionary theory, mixed infections resulted in increased anaemia. The increased anaemia was, however, not correlated with any discernable parasite trait (e.g. parasite density) or with increased transmission. CONCLUSIONS: We found some evidence supporting the hypothesis that there is an adaptive basis correlating virulence (as defined by host mortality) and transmission success in malaria parasites. This confirms the validity of applying evolutionary virulence theory to biomedical research and adds support to the prediction that partially effective vaccines may select for increasingly virulent malaria parasite strains. By contrast, there was no consistent correlation between transmission and sub-lethal anaemia, a more common outcome of malaria infection. However, overall, the data are not inconsistent with the recent proposal that sub-lethal effects may impose an upper limit on virulence. Moreover, clone specific differences in transmission phenotypes linked to anaemia do suggest that there is considerable adaptive potential relating anaemia and transmission that may lead to uncertain consequences following intervention strategies.

Adaptation, Physiological↗
PubMed2006

The use of comparative genomic hybridization to characterize genome dynamics and diversity among the serotypes of Shigella.

BACKGROUND: Compelling evidence indicates that Shigella species, the etiologic agents of bacillary dysentery, as well as enteroinvasive Escherichia coli, are derived from multiple origins of Escherichia coli and form a single pathovar. To further understand the genome diversity and virulence evolution of Shigella, comparative genomic hybridization microarray analysis was employed to compare the gene content of E. coli K-12 with those of 43 Shigella strains from all lineages. RESULTS: For the 43 strains subjected to CGH microarray analyses, the common backbone of the Shigella genome was estimated to contain more than 1,900 open reading frames (ORFs), with a mean number of 726 undetectable ORFs. The mosaic distribution of absent regions indicated that insertions and/or deletions have led to the highly diversified genomes of pathogenic strains. CONCLUSION: These results support the hypothesis that by gain and loss of functions, Shigella species became successful human pathogens through convergent evolution from diverse genomic backgrounds. Moreover, we also found many specific differences between different lineages, providing a window into understanding bacterial speciation and taxonomic relationships.

DNA, Bacterial↗