Evolution of cyclic sexual reproduction under host-parasite interactions

Alternate changes of sexual and asexual generations was studied theoretically by numerical analyses, from the viewpoint of host-parasite infective interactions. The host species was considered a diploid organism, characterized by two loci determining parasite resistance type and sexual strategy, between which a linkage exists to a certain degree. The sexual reproductive strategy was assumed to be determined by three alleles: asexual, complete sexual and cyclic sexual alleles. The effect of the parasites was represented by decreasing fitness functions of each host-type frequency. Numerical analyses of various linkages between genes and frequency dependence of host fitness revealed that the dynamics varied depending on whether the cyclic sexual allele was dominant or recessive against the complete sexual allele. When the cyclic sexual allele was dominant, the cyclic sexual strain persisted under intermediate frequency dependence of host fitness. On the other hand, when the cyclic sexual allele was recessive, it always tended to spread and to be maintained in the population. In such situations, both complete and cyclic sexual strains coexist, but the asexual strain is lost.     

Genetics of host-parasite interactions

The evolution of host susceptibility or resistance to parasites has important consequences for the evolution of parasite virulence, host sexual selection, population dynamics of both host and parasite populations, and programs of biological control. The general observation of a fraction of Individuals within a population that is not parasitized, and/or the variability in parasite intensity among hosts, may reflect several phenomena acting at different levels of ecological organization. Yet, host-parasite coevolution requires host susceptibility and parasite virulence to be genetically variable. In spite of evolutionary and epidemiological implications of genetic heterogeneities in host-parasite systems, evidence concerning natural populations is still scarce. Here, we wish to emphasize why we need a better knowledge of the genetics of host-parasite interaction in natural populations and to review the evidence concerning the heritability of host susceptibility or resistance to parasites in natural populations of animals.     

Population fluctuation in the system of host-parasite interaction

---

Contributions from the Entomological Laboratory, Kyoto University, No. 226.     

Micro-autoradiographic studies on host-parasite interactions

Tritium labeled uredospores of Uromyces phaseoli were produced be feeding the host, Phaseolus vulgaris, with ³H-orotic acid. These spores were allowed to germinate on and to penetrate into a bean leaf. 24 hrs after inoculation, the bean rust had formed the first haustorium. All fungal structures, including the fungus walls, were heavily labeled. No label could be detected in the cells that had come into contact with the hyphae. In the infected host cell, the haustorium was labeled heavily, but the sheath around the haustorium and the host cell remained free of label. These results indicate that no detectable amounts of label leach from the bean rust into the host at this stage of infection although it is known that the rust takes up many metabolites. Since the sheath remains free of label and all fungal structures are evenly labeled, it is concluded that the sheath is formed by the host.     

How selection affects phenotypic fluctuation

The large degree of phenotypic fluctuation among isogenic cells highlighted by recent studies on stochastic gene expression confers fitness on some individuals through a ‘bet‐hedging’ strategy, when faced with different selective environments. Under a single selective environment, the fluctuation may be suppressed through evolution, as it prevents maintenance of individuals around the fittest state and/or function. However, as fluctuation can increase phenotypic diversity, similar to mutation, it may contribute to the survival of individuals even under a single selective environment. To discuss whether the fluctuation increases over the course of evolution, cycles of mutation and selection for higher GFP fluorescence were carried out in Escherichia coli. Mutant genotypes possessing broad GFP fluorescence distributions with low average values emerged under strong selection pressure. These ‘broad mutants’ appeared independently on the phylogenetic tree and increased fluctuations in GFP fluorescence were attributable to the variance in mRNA abundance. In addition to the average phenotypic change by genetic mutation, the observed increase in phenotypic fluctuation acts as an evolutionary strategy to produce an extreme phenotype under severe selective environments.     

Helminth C-type lectins and host-parasite interactions

C-type lectins (C-TLs) are a family of carbohydrate-binding proteins intimately involved in diverse processes including vertebrate immune cell signalling and trafficking, activation of innate immunity in both vertebrates and invertebrates, and venom-induced haemostasis. Helminth C-TLs sharing sequence and structural similarity with mammalian immune cell lectins have recently been identified from nematode parasites, suggesting clear roles for these proteins at the host-parasite interface, notably in immune evasion. Here, Alex Loukas and Rick Maizels review the status of helminth lectin research and suggest ways in which parasitic worms might utilize C-TLs during their life history.     

Chemokines in host-parasite interactions in leishmaniasis

Crucial to the defense against leishmaniasis is the ability of the host to mount a cell-mediated immune response capable of controlling and/or eliminating the parasite. Cell recruitment to the site of infection is essential to the development of the host cellular immune response. The process is controlled by chemokines, which are chemotactic cytokines produced by leukocytes and tissue cells.     

Coevolution: Mathematical analysis of host-parasite interactions

An SIS epidemic transmitted by two similar strains of parasite acting on a host population of three genotypes which differ in their reaction to the disease is modelled and analyzed. Singular perturbation techniques are used to reduce the original system of nine differential equations to a coupled system of two equations describing the slowtime coevolution of gene frequency and parasite strain frequency.Karen Christine Beck died June 25, 1983 at home.Born February 8, 1952 in Madison, Wisconsin, She received a B.A. degree in 1974 from Luther College, Decorah, Iowa and a Ph.D. in mathematics in 1980 from the University of Iowa. Since that time she has been an instructor in the Mathematics Department at the University of Utah. She was to become an Assistant Professor at the University of Texas, Arlington, beginning Autumn, 1983. Dr. Beck's areas of specialization in mathematics were Mathematical Analysis and Mathematical Biology. She published numerous research articles that resolved various problems in these areas.     

Stability of genetic polymorphism in host-parasite interactions

Allelic diversity is common at host loci involved in parasite recognition, such as the major histocompatibility complex in vertebrates or gene-for-gene relationships in plants, and in corresponding loci encoding antigenic molecules in parasites. Diverse factors have been proposed in models to account for genetic polymorphism in host-parasite recognition. Here, a simple but general theory of host-parasite coevolution is developed. Coevolution implies the existence of indirect frequency-dependent selection (FDS), because natural selection on the host depends on the frequency of a parasite gene, and vice versa. It is shown that polymorphism can be maintained in both organisms only if there is negative, direct FDS, such that the strength of natural selection for the host resistance allele, the parasite virulence allele or both declines with increasing frequency of that allele itself. This condition may be fulfilled if the parasite has more than one generation in the same host individual, a feature which is common to most diseases. It is argued that the general theory encompasses almost all factors previously proposed to account for polymorphism at corresponding host and parasite loci, including those controlling gene-for-gene interactions.     

Leishmania donovani flagellum-specific epitopes mediating host-parasite interactions

Abstract Monoclonal antibodies were developed against flagellar components of promastigotes of Leishmania donovani . The monoclonal antibody produced by clone A₁₁ (mAb A₁₁) recognised epitopes in the polypeptides with molecular weights of 86, 66 and weakly 53 kDa. These epitopes were found to be distributed along the flagellum and at the anterior end of promastigotes. The mAb A₁₁ of IgG₁ isotype strongly agglutinated the promastigotes of L. donovani . The prior treatment of promastigotes of L. donovani with mAb A₁₁ resulted in a significant ( P < 0.001) reduction in the attachment of promastigotes to cultured mouse peritoneal macrophages of line J774G8. The affinity-purified epitopes identified by mAb A₁₁ were recognised by human sera of cases of visceral leishmaniasis. The present study suggest that flagellar-specific epitopes mediate host-parasite interactions and, therefore, the role of these epitopes in the disease process is speculated.     

Heterogeneous interspecific interactions in a host-parasite system

Macroparasites of vertebrates usually occur in multi-species communities, producing infections whose outcome in individual hosts or host populations may depend on the dynamics of interactions amongst the different component species. Within a single co-infection, competition can occur between conspecific and heterospecific parasite individuals, either directly or via the host's physiological and immune responses. We studied a natural single-host, multi-parasite model infection system (polystomes in the anuran Xenopus laevis victorianus) in which the parasite species show total interspecific competitive exclusion as adults in host individuals. Multi-species infection experiments indicated that competitive outcomes were dependent on infection species composition and strongly influenced by the intraspecific genetic identity of the interacting organisms. Our results also demonstrate the special importance of temporal heterogeneity (the sequence of infection by different species) in competition and co-existence between parasite species and predict that developmental plasticity in inferior competitors, and the induction of species-specific host resistance, will partition the within-host-individual habitat over time. We emphasise that such local (within-host) context-dependent processes are likely to be a fundamental determinant of population dynamics in multi-species parasite assemblages.     

Variability and its implications for host-parasite interactions

Variability in host-parasite interactions has considerable impact on the ecology and evolution of parasites and on the epidemiology of disease. The nature of the impact depends largely on the level of ecological organization where variability occurs: variability of parasites within their individual hosts, variability of host individuals within populations, or variability of hosts and parasites among populations. In this review, Paul Schmid-Hempel and Jacob Koella give some examples of variability at each of these levels, with particular emphasis on microparasites (defined broadly as viruses, bacteria and protozoa), consider the maintenance of the variability, and describe the implications of variability for the epidemiology of disease and the ecology of host parasite associations. In particular, they describe how variability at each level of ecological organization can affect the perception of AIDS and the evolution of virulence.