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At least 109 records · Page 6Linked to original sources
PubMed2006

Pathogen relatedness affects the prevalence of within-host competition.

Although the evolutionary consequences of within-host competition among pathogens have been examined extensively, there exists a critical gap in our understanding of factors determining the prevalence of multiple infections. Here we examine the effects of relatedness among strains of the anther-smut pathogen Microbotryum violaceum on the probability of multiple infection in its host, Silene latifolia, after sequential inoculations. We found a significantly higher probability of multiple infection when interacting strains were more closely related, suggesting mechanisms of competitive exclusion that are conditional on genotypic characteristics of the strains involved. Pathogen relatedness therefore determines the prevalence of multiple infection in addition to its outcome, with important consequences for our understanding of virulence evolution and pathogen population structure and diversity.

Basidiomycota↗
PubMed2006

Genetic reassortment of infectious bursal disease virus in nature.

Infectious bursal disease virus (IBDV), a double-stranded RNA virus, is a member of the Birnaviridae family. Four pathotypes of IBDV, attenuated, virulent, antigenic variant, and very virulent (vvIBDV), have been identified. We isolated and characterized the genomic reassortant IBDV strain ZJ2000 from severe field outbreaks in commercial flocks. Full-length genomic sequence analysis showed that ZJ2000 is a natural genetic reassortant virus with segments A and B derived from attenuated and very virulent strains of IBDV, respectively. ZJ2000 exhibited delayed replication kinetics as compared to attenuated strains. However, ZJ2000 was pathogenic to specific pathogen free (SPF) chickens and chicken embryos. Similar to a standard virulent IBDV strain, ZJ2000 caused 26.7% mortality, 100% morbidity, and severe bursal lesions at both gross and histopathological levels. Taken together, our data provide direct evidence for genetic reassortment of IBDV in nature, which may play an important role in the evolution, virulence, and host range of IBDV. Our data also suggest that VP2 is not the sole determinant of IBDV virulence, and that the RNA-dependent RNA polymerase protein, VP1, may play an important role in IBDV virulence. The discovery of reassortant viruses in nature suggests an additional risk of using live IBDV vaccines, which could act as genetic donors for genome reassortment.

Amino Acid Substitution↗
PubMed2003

Dynamics of multiple infection and within-host competition by the anther-smut pathogen.

Infection of one host by multiple pathogen genotypes represents an important area of pathogen ecology and evolution that lacks a broad empirical foundation. Multiple infection of Silene latifolia by Microbotryum violaceum was studied under field and greenhouse conditions using the natural polymorphism for mating-type bias as a marker. Field transmission resulted in frequent multiple infection, and each stem of the host was infected independently. Within-host diversity of infections equaled that of nearby inoculum sources by the end of the growing season. The number of diseased stems per plant was positively correlated with multiple infection and with overwintering mortality. As a result, multiply infected plants were largely purged from the population, and there was lower within-host pathogen diversity in the second season. However, among plants with a given number of diseased stems, multiply infected plants had a lower risk of overwintering mortality. Following simultaneous and sequential inoculation, strong competitive exclusion was demonstrated, and the first infection had a significant advantage. Dynamics of multiple infection initially included components of coinfection models for virulence evolution and then components of superinfection models after systemic colonization. Furthermore, there was evidence for an advantage of genotypes with mating-type bias, which may contribute to maintenance of this polymorphism in natural populations.

Basidiomycota↗
PubMed2000

Evolution of parasite virulence against qualitative or quantitative host resistance.

We analysed the effects of two different modes of host resistance on the evolution of parasite virulence. Hosts can either adopt an all-or-nothing qualitative response (i.e. resistant hosts cannot be infected) or a quantitative form of resistance (i.e. which reduces the within-host growth rate of the parasite). We show that the mode of host resistance greatly affects the evolutionary outcome. Specifically, a qualitative form of resistance reduces parasite virulence, while a quantitative form of resistance generally selects for higher virulence.

Animals↗
PubMed2006

Virulence determinants in a natural butterfly-parasite system.

Much evolutionary theory assumes that parasite virulence (i.e. parasite-induced host mortality) is determined by within-host parasite reproduction and by the specific parasite genotypes causing infection. However, many other factors could influence the level of virulence experienced by hosts. We studied the protozoan parasite Ophryocystis elektroscirrha in its host, the monarch butterfly, Danaus plexippus. We exposed monarch larvae to wild-isolated parasites and assessed the effects of within-host replication and parasite genotype on host fitness measures, including pre-adult development time and adult weight and longevity. Per capita replication rates of parasites were high, and infection resulted in high parasite loads. Of all host fitness traits, adult longevity showed the clearest relationship with infection status, and decreased continuously with increasing parasite loads. Parasite genotypes differed in their virulence, and these differences were maintained across ecologically relevant variables, including inoculation dose, host sex and host age at infection. Thus, virulence appears to be a robust genetic parasite trait in this system. Although parasite loads and genotypes had strong effects on virulence, inoculation dose, host sex and age at infection were also important. These results have implications for virulence evolution and emphasize the need for a detailed understanding of specific host-parasite systems for addressing theory.

Animals↗
PubMed2005

Emergence of a convex trade-off between transmission and virulence.

Most models of virulence evolution assume that a parasite cannot raise its transmission rate without causing more harm to its host. However, the existence of such trade-off relationships has recently been challenged. Here, we study how a trade-off can emerge from a model that explicitly incorporates within-host dynamics. We find that the existence and the convexity of the trade-off are robust, which implies a definite level of evolutionarily stable virulence (ESV) for the parasite. However, we also show that the dependence of the ESV on parameter values may be very strong. One possible consequence of this sensitivity is that relationships between transmission and virulence observed across populations need not conform to the patterns expected on the basis of a common (fixed) trade-off. We discuss possible experiments and implications of our results for the development of virulence management strategies.

Disease Transmission, Infectious↗
PubMedDate not supplied

[Avian influenza A (H5N1) infectious in both birds and humans in South-Eastern Asian countries].

Avian influenza affects most types of birds and occurs in epidemics on poultry farms. The fatal disease is named "highly pathogenic avian influenza" and is caused by influenza A virus subtypes H5 and H7. The natural reservoir is the migratory waterfowl that occasionally infects domestic poultry. In 1997 in Hong Kong, 18 persons were infected and 6 of them died. At the end of 2003 and the beginning of 2004, avian influenza H5N1 infected numerous farms in several South-Eastern Asian countries. The virus was transmitted to humans in close contact with infected birds. A total of 34 persons were infected and 23 of them died. There is currently a considerable concern about the H5N1 avian influenza that has infected humans: the high virulence, evolution rate, the possibility of recombination with other influenza viruses, how H5N1 variants that infect humans or different approaches to the development of influenza vaccines.

Animals↗
PubMed2026

From colonization to infection: Genomic evolution of Clostridioides difficile pathogenesis.

Clostridioides difficile is a spore-forming, toxin-producing anaerobe that is a leading cause of healthcare-associated infections. Its success as a pathogen reflects a complex interplay between bacterial evolution, virulence regulation, ecological adaptation, environmental selection, and host susceptibility. Comparative genomics has revealed deep C. difficile lineage diversification, driven by mobile genetic elements and selective pressures from antibiotics and host environments. These events affect strain-specific virulence by shaping the organization and regulation of the pathogenicity toxin loci, metabolic adaptations for nutrient utilization, and enhanced spore resilience. This review integrates evolutionary and genomic perspectives to illustrate how adaptive diversification has sculpted C. difficile pathogenesis and epidemic success.

CP: microbiology↗
PubMed1994

Short-sighted evolution and the virulence of pathogenic microorganisms.

For some microorganisms, virulence may be an inadvertent consequence of mutation and selection in the parasite population, occurring within a host during the course of an infection. This type of virulence is short-sighted, in that it engenders no advantage to the pathogen beyond the afflicted host. Bacterial meningitis, poliomyelitis and AIDS are three candidates for this model of the evolution of virulence.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Epidemiology, hypermutation, within-host evolution and the virulence of Neisseria meningitidis.

Many so-called pathogenic bacteria such as Neisseria meningitidis, Haemophilus influenzae, Staphylococcus aureus and Streptococcus pneumoniae are far more likely to colonize and maintain populations in healthy individuals asymptomatically than to cause disease. Disease is a dead-end for these bacteria: virulence shortens the window of time during which transmission to new hosts can occur and the subpopulations of bacteria actually responsible for disease, like those in the blood or cerebral spinal fluid, are rarely transmitted to new hosts. Hence, the virulence factors underlying their occasional pathogenicity must evolve in response to selection for something other than making their hosts sick. What are those selective pressures? We address this general question of the evolution of virulence in the context of phase shifting in N. meningitidis, a mutational process that turns specific genes on and off, and, in particular, contingency loci that code for virulence determinants such as pili, lipopolysaccharides, capsular polysaccharides and outer membrane proteins. We use mathematical models of the epidemiology and the within-host infection dynamics of N. meningitidis to make the case that rapid phase shifting evolves as an adaptation for colonization of diverse hosts and that the virulence of this bacterium is an inadvertent consequence of short-sighted within-host evolution, which is exasperated by the increased mutation rates associated with phase shifting. We present evidence for and suggest experimental and retrospective tests of these hypotheses.

Biological Evolution↗
PubMed2001

Pathogenicity determinants in the complex virus population of a Plum pox virus isolate.

Several subisolates were separated from a single Plum pox virus (PPV) isolate, PPV-PS. In spite of an extremely high sequence conservation (more than 99.9% similarity), different subisolates differed largely in pathogenicity in herbaceous hosts and infectivity in woody plants. The severity of symptomatology did not seem to correlate with virus accumulation. Sequence analysis and site-directed mutagenesis demonstrated that single amino acid changes in the helper component (HC) protein caused a drastic effect on virus symptoms in herbaceous hosts and notably modified virus infectivity in peach seedlings. These results indicate that HC variation might play an important role in virulence evolution of natural plant virus infections. Moreover, the analysis of Potato virus X (PVX)-HC chimeras showed that the identified HC amino acid changes had parallel effects on the severity of symptoms caused by PPV and on HC-induced enhancement of PVX pathogenicity, indicating that HC functions in potyvirus symptomatology and in synergism with other viruses have overlapping determinants.

Amino Acid Substitution↗
PubMed2004

Mixed inoculations of a microsporidian parasite with horizontal and vertical infections.

Mixed infections, where more than one parasite genotype is present in a single host, have been suggested to be an important factor in host-parasite interactions. As the host represents a limited resource, co-infecting parasite genotypes are expected to be under resource competition. Competition will not only modify the survival of the co-infecting genotypes, but is also likely to affect total within-host parasite growth as well as host survival and reproduction. We measured parasite infectivity and spore production of seven isolates of Octosporea bayeri (Microsporidia) and their effect on the reproduction and longevity of its host Daphnia magna (Cladocera), after single- or double-isolate inoculations through vertical and horizontal transmission. Double-isolate inoculations increased parasite infectivity and total spore production in horizontal infections, but had no significant effect on host reproduction or longevity. The increase in spore production in double-isolate inoculations was not found when infections occurred vertically. Our results suggest that, depending on the way the infection was acquired, within-host reproduction can increase as a result of parasite genetic diversity, without necessarily affecting the host's fitness. Whether this challenges the current views of virulence evolution depends on the definitions used.

Animals↗
PubMed2006

Detecting genetic variability among different Mycobacterium tuberculosis strains using DNA microarrays technology.

Recent advances in functional and comparative genomics have improved our understanding of genetic diversity among the Mycobacterium tuberculosis complex. In this study, we investigated the genetic polymorphism of M. tuberculosis using whole-genome microarray analysis. Amplified fragments of 15 M. tuberculosis strains (from two different geographical origins) and the reference strain H37Rv were produced by random amplification of polymorphic DNA (RAPD) using three different primers. The RAPD products were labeled with fluorescent dyes (Cy3 and Cy5) and hybridized to a TB DNA microarray representing nearly all open reading frames (ORFs) of H37Rv. The final results were analyzed using bioinformatic tools. Some genetic variability was found among the 16 M. tuberculosis strains. The majority of the highly polymorphic DNA sequences were observed in ORFs representing non-essential genes of the bacterium. The future use of comparative genomics based on DNA microarray technology should prove a powerful tool for understanding phenotypic variability among M. tuberculosis isolates of similar genetic composition. It is also a promising approach to provide important insights into evolution, virulence and pathogenesis of M. tuberculosis.

DNA, Bacterial↗
PubMed2006

The impact of imperfect vaccines on the evolution of HIV virulence.

A theoretical framework is proposed on which some hypotheses related to the impact of imperfect vaccines on the evolution of HIV virulence can be tested. For this, a linear increase of risk behaviour with vaccine efficacy is assumed. This is based on the hypothesis that people are prone to relax preventive measures by knowing that they and their partners are vaccinated and that this effect is more intense the more effective the vaccine is known to be. An additional, and perhaps more important hypothesis is related to the theoretical possibility that increased risk behaviour of some vaccinated individuals in partially protected populations could act as a selective pressure toward more virulent HIV strains. Those hypotheses were tested by a mathematical model that considers three different HIV strains competing against each other in a population partially protected by imperfect vaccines of distinct efficacies. Simulations of the model demonstrated that, under the above hypotheses, there is a shift in HIV virulence towards more aggressive strains with increase in vaccine efficacy, associated with a marked reduction in the total amount of transmission and, consequently, in the prevalence of HIV. Potential ways for further testing the theory/model and the implications of the results are discussed.

AIDS Vaccines↗
PubMed1989

Host density and the evolution of parasite virulence.

Social and cultural habits of human populations affect the biological evolution of the agents of infectious diseases. Measles and similar diseases have evolved in the Old World and cannot have existed in their present form before the rise of the great river valley civilizations. It is suggested that increased virulence of measles in white and indigenous communities in America 1500-1800 may be due to a rare strain of the virus, which was selected during transfer from Europe. The release of viruses for biological pest control has provided new material for the study of the co-evolution of host-parasite systems, which has upset the dogma "evolution tends to avirulence". It is pointed out that this issue is closely related to the group selection debate among ethologists, i.e. to the problem: how can group selection overcome individual selection? A model is proposed in which differential growth of two strains of a parasite within the host and their transmission to new hosts is considered. It is supposed that transmission stages excreted by infectious hosts enter a common pool where they are mixed before infecting new hosts. Under these conditions, selection of the slower strain is possible only if the mean size of parasite inoculum is very small, i.e. if the density of transmission stages in the environment is low. The impact of this result on host pathology depends on the relation between virulence and transmission efficiency of the parasite.

Animals↗
PubMed2002

Mixed strain schistosome infections of snails and the evolution of parasite virulence.

Mathematical models often propose that within-host competition between parasites can be a major factor in the evolution of increased parasite virulence. Kin selection predicts that as the coefficient of relatedness between infecting parasites decreases, the benefits of competition to individual genotypes increases. Thus where parasites can adjust their behaviour in response to current conditions, higher virulence is predicted in multiple genotype infections. There is limited experimental data, however, regarding the effects of mixed strain infections on host and parasite fitness. We investigated, for a snail-schistosome system, whether a conditional increase in replication rates occurred in mixed genotype infections and resulted in increased virulence. Four groups of Biomphalaria glabrata snails were exposed to 1 or 2 laboratory strains of Schistosoma mansoni. Mixed genotype infections were observed to be more virulent than single genotype infections, in terms of reductions in host reproductive success and survival. Parasite reproductive rate was also increased in mixed strain groups. Reduced host reproductive success was suggested to be directly due to the genetic heterogeneity of the parasitic infections resulting in increased host defence costs. Reduced host survival was consistent with an adaptive conditional parasite response.

Animals↗
PubMed2003

Mosquito mortality and the evolution of malaria virulence.

Several laboratory studies of malaria parasites (Plasmodium sp.) and some field observations suggest that parasite virulence, defined as the harm a parasite causes to its vertebrate host, is positively correlated with transmission. Given this advantage, what limits the continual evolution of higher parasite virulence? One possibility is that while more virulent strains are more infectious, they are also more lethal to mosquitoes. In this study, we tested whether the virulence of the rodent malaria parasite P. chabaudi in the laboratory mouse was correlated with the fitness of mosquitoes it subsequently infected. Mice were infected with one of seven genetically distinct clones of P. chabaudi that differ in virulence. Weight loss and anemia in infected mice were monitored for 16-17 days before Anopheles stephensi mosquitoes were allowed to take a blood meal from them. Infection virulence in mice was positively correlated with transmission to mosquitoes (infection rate) and weakly associated with parasite burden (number of oocysts). Mosquito survival fell with increasing oocyst burden, but there was no overall statistically significant relationship between virulence in mice and mosquito mortality. Thus, there was no evidence that more virulent strains are more lethal to mosquitoes. Both vector survival and fecundity depended on parasite clone, and contrary to expectations, mosquitoes fed on infections more virulent to mice were more fecund. The strong parasite genetic effects associated with both fecundity and survival suggests that vector fitness could be an important selective agent shaping malaria population genetics and the evolution of phenotypes such as virulence in the vector.

Animals↗