What's good for the host is good for the bug

Tuberculosis, caused by Mycobacterium tuberculosis, kills approximately two million people each year. The infection is characterized by an inflammatory response culminating in the formation of a granuloma, a collection of immune cells that controls the infection. However, the granuloma can be the source of immunopathology that encourages transmission. Recent data support the idea that mycobacterial products can positively and negatively regulate the inflammatory response. Our contention is that induction of the immune response and subsequent granuloma formation is beneficial to the host for control of infection, and is also beneficial to the bacillus, as a place to hide and as a means for transmitting the infection to naive hosts.     

Protein targeting from malaria parasites to host erythrocytes

Malaria is caused by obligate intracellular parasites, which live in host erythrocytes and remodel these cells to provide optimally for their own needs. Plasmodium falciparum, responsible for malaria in humans, transports many proteins into erythrocytes which help the parasite survive in the host. The recent discovery of a host cell-targeting sequence present in both soluble and transmembrane P. falciparum proteins provoked a discussion on the potential mechanisms of parasite protein entry into infected erythrocytes which is summarized here.     

Mitochondrial dynamics: to be in good shape to survive

Mitochondria are essential organelles of all eukaryotic cells that play a key role in several physiological processes and are involved in the pathology of many diseases. These organelles form a highly dynamic network, which results from continuous fusion and fission processes. Importance of these processes is underlined by inherited human diseases caused by mutations in two mitochondrial pro-fusion genes: Charcot-Marie-Tooth disease, caused by mutations in Mitofusin 2 gene and ADOA due to mutations in OPA1. During apoptosis, the mitochondrial network is disintegrated and the outer mitochondrial membrane permeabilized, which results in the release of several apoptogenic proteins, including cytochrome c. Although modulating mitochondrial fusion and fission machineries has been reported to influence the apoptotic response to various stimuli, it is still unclear whether fission is absolutely required for apoptosis. In this review, we present the latest progress in the field of mitochondrial dynamics with a particular emphasis on its implication in apoptosis and in diseases.     

Individual recognition: it is good to be different

Individual recognition (IR) behavior has been widely studied, uncovering spectacular recognition abilities across a range of taxa and modalities. Most studies of IR focus on the recognizer (receiver). These studies typically explore whether a species is capable of IR, the cues that are used for recognition and the specializations that receivers use to facilitate recognition. However, relatively little research has explored the other half of the communication equation: the individual being recognized (signaler). Provided there is a benefit to being accurately identified, signalers are expected to actively broadcast their identity with distinctive cues. Considering the prevalence of IR, there are probably widespread benefits associated with distinctiveness. As a result, selection for traits that reveal individual identity might represent an important and underappreciated selective force contributing to the evolution and maintenance of genetic polymorphisms.     

How to survive in the host: the Yersinia lesson

The Yop virulon allows Yersinia spp. to resist the immune response of the host by injecting harmful proteins into host cells. It is composed of four elements: (i) type III secretion machinery called Ysc; (ii) a set of proteins required to translocate the effector proteins inside the eukaryotic cells; (iii) a control system, and (iv) six Yop effector proteins.     

Cryptosporidia: epicellular parasites embraced by the host cell membrane

The ultrastructure of two gastric cryptosporidia, Cryptosporidium muris from experimentally infected rodents (Mastomys natalensis) and Cryptosporidium sp. 'toad' from naturally infected toads (Duttaphrynus melanostictus), was studied using electron microscopy. Observations presented herein allowed us to map ultrastructural aspects of the cryptosporidian invasion process and the origin of a parasitophorous sac. Invading parasites attach to the host cell, followed by gradual envelopment, with the host's cell membrane folds, eventually forming the parasitophorous sac. Cryptosporidian developmental stages remain epicellular during the entire life cycle. The parasite development is illustrated in detail using high resolution field emission scanning electron microscopy. This provides a new insight into the ultrastructural detail of host-parasite interactions and species-specific differences manifested in frequency of detachment of the parasitophorous sac, radial folds of the parasitophorous sac and stem-formation of the parasitised host cell.     

How to analyse host discrimination

Abstract. 1. Two usual definitions of host discrimination are presented. The first is 'the ability of a parasite to distinguish unparasitized from parasitized hosts and to lay eggs in the former'. This definition is not useful and even confusing since it does not include the ability of a parasite to distinguish hosts containing different numbers of parasite eggs and to lay preferably only in those with the lowest numbers.
2. The second definition is 'the ability of a parasite to distribute its eggs in a non-random, regular way among its hosts'. It is argued that most field data are insufficient to permit any conclusions about host discriminative ability on the basis of this definition. An example is given of an apparent random distribution by parasites that are perfectly able to discriminate.
3. Arguments are given for studying the behaviour of the parasite in order to answer the question of host discrimination. Five examples of parasites are presented that would erroneously have been classified as non-discriminators on the basis of the first definition, since they all superparasitize.
4. It is suggested that the meaning of the term 'host discrimination' be extended to include the ability of a parasite to distinguish hosts with different numbers of eggs.     

Conservatism of host specificity in parasites

As information becomes available for many groups of organisms a general pattern of phylogenetic conservatism in ecological characters or morphological traits is now widely recognized. Conversely, conservatism of external ecological attributes throughout a lineage is still a contentious theme in ecology. Moreover, the studies exploring this topic have focused on free-living organisms, and have ignored parasites. The main external ecological attribute of parasite species is certainly their host specificity, which is a key determinant of both their range size and local abundance. We address the subject of conservatism and predictability of host specificity using 2 large databases concerning, respectively, ectoparasites and endoparasites. We found a significant positive relationship between the numbers of host species infested by flea sister species. Moreover, this result was consistent whether we used sympatric or allopatric flea species, suggesting no influence of the mode of speciation on this conservatism of specificity. Additionally, our results showed that congeneric helminth species have more similar host taxonomic diversities than expected by chance, although this conservatism is due mostly to trematodes. Whilst there is evidence of conservatism, the moderate levels preclude robust prediction of host specificity for one species based on that of closely related species.     

How to invade,replicate, and escape from host organisms. A challenge in defining virulence factors for parasites

During millions of years, parasites have been adapting to different environments and hosts. During this time, they have acquired different molecules and peculiar structures, some absent in other living organisms, in order to successfully invade hosts, resist immune attack, and proliferate in the hosts. Nowadays, several genome sequences and a multitude of new information have been generated for many human and animal parasites, opening new possibilities for understanding in detail how they interact with the host and cause disease. Investigations of these molecules and the associated structures, together with their functional roles, are now emerging, providing key advances in understanding pathology that could be used for developing robust strategies to selectively target the parasites without damaging the host.     

Adaptation of gastrointestinal nematode parasites to host genotype: single locus simulation models

Background

Breeding livestock for improved resistance to disease is an increasingly important selection goal. However, the risk of pathogens adapting to livestock bred for improved disease resistance is difficult to quantify. Here, we explore the possibility of gastrointestinal worms adapting to sheep bred for low faecal worm egg count using computer simulation. Our model assumes sheep and worm genotypes interact at a single locus, such that the effect of an A allele in sheep is dependent on worm genotype, and the B allele in worms is favourable for parasitizing the A allele sheep but may increase mortality on pasture. We describe the requirements for adaptation and test if worm adaptation (1) is slowed by non-genetic features of worm infections and (2) can occur with little observable change in faecal worm egg count.

Results

Adaptation in worms was found to be primarily influenced by overall worm fitness, viz. the balance between the advantage of the B allele during the parasitic stage in sheep and its disadvantage on pasture. Genetic variation at the interacting locus in worms could be from de novo or segregating mutations, but de novo mutations are rare and segregating mutations are likely constrained to have (near) neutral effects on worm fitness. Most other aspects of the worm infection we modelled did not affect the outcomes. However, the host-controlled mechanism to reduce faecal worm egg count by lowering worm fecundity reduced the selection pressure on worms to adapt compared to other mechanisms, such as increasing worm mortality. Temporal changes in worm egg count were unreliable for detecting adaptation, despite the steady environment assumed in the simulations.

Conclusions

Adaptation of worms to sheep selected for low faecal worm egg count requires an allele segregating in worms that is favourable in animals with improved resistance but less favourable in other animals. Obtaining alleles with this specific property seems unlikely. With support from experimental data, we conclude that selection for low faecal worm egg count should be stable over a short time frame (e.g. 20 years). We are further exploring model outcomes with multiple loci and comparing outcomes to other control strategies.     

On the role of host phenotypic plasticity in host shifting by parasites

Ecological speciation appears to contribute to the diversification of insect herbivores and other parasites, which together comprise a major component of Earth's biodiversity. Host shifts are likely an important step in ecological speciation, and understanding how such shifts occur is critical to forming and testing hypotheses explaining parasite diversity. In this article, I argue that phenotypic variation in hosts arising from environmental variation (phenotypic plasticity) can promote shifts in parasites by bridging both spatiotemporal and phenotypic gaps between ancestral and novel hosts. This hypothesis, which I call the ‘plastic‐bridge hypothesis’, is conceptually distinct from those invoking genetic variation in bridging these gaps. I describe the mechanistic basis of plastic bridges, review circumstantial evidence in support of the hypothesis and suggest strategies for testing it. I use herbivorous insects and their host plants as a model, but the proposed ideas apply to any system fitting a broad definition of a host‐parasite relationship. The plastic‐bridge perspective suggests that parasite diversity is not only due to divergent selection provided by hosts, but also to the intraspecific variation that facilitates shifts between them. This view is timely, as biological invasion and range shifts associated with climate change foster novel interactions between parasites and hosts.     

Immunological synapses: breaking up may be good to do

Activated T cells form stable immunological synapses with antigen-presenting cells whereas na?ve T cells initially engage in more transient interactions. Sims et al. (2007) demonstrate that these transient interactions are due to the kinase PKCtheta, which serves to destabilize the synapse thereby permitting T cells to migrate elsewhere. They also show that re-establishment of a synapse involves the actin regulator WASp.     

Acyltransferases in plants: a good time to be BAHD

Acylation is a common and biochemically significant modification of plant secondary metabolites. Plant BAHD acyltransferases constitute a large family of acyl CoA-utilizing enzymes whose products include small volatile esters, modified anthocyanins, as well as constitutive defense compounds and phytoalexins. The catalytic versatility of BAHD enzymes makes it very difficult to make functional predictions from primary sequence alone. Recent advances in genome sequencing and the availability of the first crystal structure of a BAHD member are, however, providing insights into the evolution and function of these acyltransferases within the plant kingdom.