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Virtually all plants and animals, including humans, are home to symbiotic microorganisms. Symbiotic interactions can be neutral, harmful or have beneficial effects on the host organism. However, growing evidence suggests that microbial symbionts can evolve rapidly, resulting in drastic transitions along the parasite–mutualist continuum. In this Review, we integrate theoretical and empirical findings to discuss the mechanisms underpinning these evolutionary shifts, as well as the ecological drivers and why some host–microorganism interactions may be stuck at the end of the continuum. In addition to having biomedical consequences, understanding the dynamic life of microorganisms reveals how symbioses can shape an organism’s biology and the entire community, particularly in a changing world.Symbiotic interactions can be neutral, harmful or have beneficial effects for host organisms. In this Review, Drew, Stevens and King discuss the evolutionary transitions of host–microorganism symbioses along the parasite–mutualist continuum, the mechanisms underlying evolutionary changes, the selective pressures involved and common empirical approaches for studying them.

Many plants use environmental cues, including seasonal changes of day length (photoperiod), to control their flowering time. Under inductive conditions, FLOWERING LOCUS T (FT) protein is synthesized in leaves, and FT protein is a mobile signal, which is able to travel to the shoot apex to induce flowering. Dodders (Cuscuta, Convolvulaceae) are root- and leafless plants that parasitize a large number of autotrophic plant species with varying flowering time. Remarkably, some dodder species, e.g., Cuscuta australis, are able to synchronize their flowering with the flowering of their hosts. Detailed sequence inspection and expression analysis indicated that the FT gene in dodder C. australis very likely does not function in activating flowering. Using soybean host plants cultivated under inductive and noninductive photoperiod conditions and soybean and tobacco host plants, in which FT was overexpressed and knocked out, respectively, we show that FT-induced flowering of the host is likely required for both host and parasite flowering. Biochemical analysis revealed that host-synthesized FT signals are able to move into dodder stems, where they physically interact with a dodder FD transcription factor to activate dodder flowering. This study demonstrates that FTs can function as an important interplant flowering signal in host–dodder interactions. The unique means of flowering regulation of dodder illustrates how regressive evolution, commonly found in parasites, may facilitate the physiological synchronization of parasite and host, here allowing the C. australis parasite to time reproduction exactly with that of their hosts, likely optimizing parasite fitness.

Key Points By producing antibodies, B cells are main players in the protective immune response against pathogenic infections. In response to antigens, they mature into antibody-producing plasma cells or into memory B cells, which can quickly be reactivated following secondary challenge. Several parasites, viruses and bacteria that affect human health worldwide interact directly with and manipulate B cell functions. This direct targeting occurs in addition to the indirect effects on the infection-induced local microenvironment and shows the diversity of mechanisms used by pathogens to evade host-protective immunity. Some pathogens use B cells as a reservoir and use virulence factors to facilitate invasion. This pathogenic manipulation mechanism is used to support pathogen survival in the host or dissemination of the infection. The induction of polyclonal B cell activation and the production of low-specificity antibodies are often associated with an early blunting of infections, but can also dilute pathogen-specific antibody responses. Some pathogens have evolved mechanisms to deliberately induce the production of low-specificity antibodies by direct interaction with B cells in order to subvert specific immune responses. Regulatory B cells are B cells that secrete immunosuppressive cytokines, thereby modulating protective T cell responses. A number of pathogens selectively induce regulatory B cell functions by direct interaction to suppress the establishment of protective immunity. An intricate balance of signalling pathways decides whether a B cell lives or dies during antigen-dependent maturation. Some pathogens have evolved mechanisms to induce B cell death, thereby eliminating the cell population that confers protective immunity. Some pathogens induce the survival of B cells by direct interaction. Although this seems detrimental at first glance, they often simultaneously hide intracellularly in B cells or divert protective antibody responses. The elucidation of cellular mechanisms in the establishing and diversion of protective B cell responses could lead to new therapeutic and vaccination approaches in future. To achieve this, pathogens should not be used as a mere tool to analyse immune responses, but in combination with systems biology, in vitro and in vivo studies should be carried out to characterize B cell responses and pathogenic mechanisms of immune diversion. B cells are essential components of the immune response against infection. However, several bacteria, viruses and parasites are able to infect B cells and manipulate B cell functions and survival. Here, the authors review how pathogens use B cells as reservoirs, manipulate B cell differentiation and interfere with B cell survival, and they discuss the implications for ongoing immune responses. B cells have long been regarded as simple antibody production units, but are now becoming known as key players in both adaptive and innate immune responses. However, several bacteria, viruses and parasites have evolved the ability to manipulate B cell functions to modulate immune responses. Pathogens can affect B cells indirectly, by attacking innate immune cells and altering the cytokine environment, and can also target B cells directly, impairing B cell-mediated immune responses. In this Review, we provide a summary of recent advances in elucidating direct B cell–pathogen interactions and highlight how targeting this specific cell population benefits different pathogens.

Obligate intracellular Apicomplexa parasites share a unique invasion mechanism involving a tight interaction between the host cell and the parasite surfaces called the moving junction (MJ). The MJ, which is the anchoring structure for the invasion process, is formed by secretion of a macromolecular complex (RON2/4/5/8), derived from secretory organelles called rhoptries, into the host cell membrane. AMA1, a protein secreted from micronemes and associated with the parasite surface during invasion, has been shown in vitro to bind the MJ complex through a direct association with RON2. Here we show that RON2 is inserted as an integral membrane protein in the host cell and, using several interaction assays with native or recombinant proteins, we define the region that binds AMA1. Our studies were performed both in Toxoplasma gondii and Plasmodium falciparum and although AMA1 and RON2 proteins have diverged between Apicomplexa species, we show an intra-species conservation of their interaction. More importantly, invasion inhibition assays using recombinant proteins demonstrate that the RON2-AMA1 interaction is crucial for both T. gondii and P. falciparum entry into their host cells. This work provides the first evidence that AMA1 uses the rhoptry neck protein RON2 as a receptor to promote invasion by Apicomplexa parasites.

One of the most striking outcomes of coevolution between species is egg mimicry by brood parasitic birds, resulting from rejection behavior by discriminating host parents. Yet, how exactly does a host detect a parasitic egg? Brood parasitism and egg rejection behavior provide a model system for exploring the relative importance of different visual cues used in a behavioral task. Although hosts are discriminating, we do not know exactly what cues they use, and to answer this it is crucial to account for the receiver's visual perception. Color, luminance (\"perceived lightness\") and pattern information have never been simultaneously quantified and experimentally tested through a bird's eye. The cuckoo finch Anomalospiza imberbis and its hosts show spectacular polymorphisms in egg appearance, providing a good opportunity for investigating visual discrimination owing to the large range of patterns and colors involved. Here we combine field experiments in Africa with modeling of avian color vision and pattern discrimination to identify the specific visual cues used by hosts in making rejection decisions. We found that disparity between host and foreign eggs in both color and several aspects of pattern (dispersion, principal marking size, and variability in marking size) were important predictors of rejection, especially color. These cues correspond exactly to the principal differences between host and parasitic eggs, showing that hosts use the most reliable available cues in making rejection decisions, and select for parasitic eggs that are increasingly mimetic in a range of visual attributes.

Information on parasites and disease in marine ecosystems lags behind terrestrial systems, increasing the challenge of predicting responses of marine host–parasite systems to climate change. However, here I examine several generalizable aspects and research priorities. First, I advocate that quantification and comparison of host and parasite thermal performance curves is a smart approach to improve predictions of temperature effects on disease. Marine invertebrate species are ectothermic and should be highly conducive to this approach given their generally short generation times. Second, in marine systems, shallow subtidal and intertidal areas will experience the biggest temperature swings and thus likely see the most changes to host–parasite dynamics. Third, for some responses like parasite intensity, as long as the lethal limit of the parasite is not crossed, on average, there may be a biological basis to expect temperature-dependent intensification of impacts on hosts. Fourth, because secondary mortality effects and indirect effects of parasites can be very important, we need to study temperature effects on host–parasite dynamics in a community context to truly know their bottom line effects. This includes examining climate-influenced effects of parasites on ecosystem engineers given their pivotal role in communities. Finally, other global change factors, especially hypoxia, salinity, and ocean acidity, covary with temperature change and need to be considered and evaluated when possible for their contributing effects on host–parasite systems. Climate change–disease interactions in nearshore marine environments are complex; however, generalities are possible and continued research, especially in the areas outlined here, will improve our understanding.

Altered thermal regimes associated with climate change are impacting significantly on the physical, chemical, and biological characteristics of the Earth’s natural ecosystems, with important implications for the biology of aquatic organisms. As well as impacting the biology of individual species, changing thermal regimes have the capacity to mediate ecological interactions between species, and the potential for climate change to impact host–parasite interactions in aquatic ecosystems is now well recognized. Predicting what will happen to the prevalence and intensity of infection of parasites with multiple hosts in their life cycles is especially challenging because the addition of each additional host dramatically increases the potential permutations of response. In this short review, we provide an overview of the diverse routes by which altered thermal regimes can impact the dynamics of multi-host parasite life cycles in aquatic ecosystems. In addition, we examine how experimentally amenable host–parasite systems are being used to determine the consequences of changing environmental temperatures for these different types of mechanism. Our overarching aim is to examine the potential of changing thermal regimes to alter not only the biology of hosts and parasites, but also the biology of interactions between hosts and parasites. We also hope to illustrate the complexity that is likely to be involved in making predictions about the dynamics of infection by multi-host parasites in thermally challenged aquatic ecosystems.

Parasites have long been thought to influence the evolution of migration, but precisely determining the conditions under which this occurs by quantifying costs of infection remains a challenge. Here we developed a model that demonstrates how the metric used to describe infection (richness/diversity, prevalence or intensity) shapes the prediction of whether migration will evolve. The model shows that predictions based on minimizing richness yield opposite results compared to those based on minimizing prevalence, with migration only selected for when minimizing prevalence. Consistent with these findings, empirical studies that measure parasite diversity typically find that migrants are worse off than residents, while those measuring prevalence or intensity find the opposite. Our own empirical analysis of fish parasite data finds that migrants (of all types) have higher parasite richness than residents, but with no significant difference in either prevalence or intensity.

Background Increasing temperatures are predicted to strongly impact host-parasite interactions, but empirical tests are rare. Host species that are naturally exposed to a broad temperature spectrum offer the possibility to investigate the effects of elevated temperatures on hosts and parasites. Using three-spined sticklebacks, Gasterosteus aculeatus L., and tapeworms, Schistocephalus solidus (Müller, 1776), originating from a cold and a warm water site of a volcanic lake, we subjected sympatric and allopatric host-parasite combinations to cold and warm conditions in a fully crossed design. We predicted that warm temperatures would promote the development of the parasites, while the hosts might benefit from cooler temperatures. We further expected adaptations to the local temperature and mutual adaptations of local host-parasite pairs. Results Overall, S. solidus parasites grew faster at warm temperatures and stickleback hosts at cold temperatures. On a finer scale, we observed that parasites were able to exploit their hosts more efficiently at the parasite’s temperature of origin. In contrast, host tolerance towards parasite infection was higher when sticklebacks were infected with parasites at the parasite’s ‘foreign’ temperature. Cold-origin sticklebacks tended to grow faster and parasite infection induced a stronger immune response. Conclusions Our results suggest that increasing environmental temperatures promote the parasite rather than the host and that host tolerance is dependent on the interaction between parasite infection and temperature. Sticklebacks might use tolerance mechanisms towards parasite infection in combination with their high plasticity towards temperature changes to cope with increasing parasite infection pressures and rising temperatures.

If every metazoan species has at least one host-specific parasite, as several local scale studies have suggested, then half of all species could be parasites. However, host specificity varies significantly depending on host phylogeny, body size, habitat, and geographic distribution. The best studied hosts tend to be vertebrates, larger animals, and/or widespread, and thus have a higher number of parasites and host-specific parasites. Thus, host specificity for these well-known taxa cannot be simply extrapolated to other taxa, notably invertebrates, small sized, and more endemic species, which comprise the major portion of yet to be discovered species. At present, parasites of animals comprise about 5% of named species. This article analyzed the rate of description of several largely parasitic taxa within crustaceans (copepods, amphipods, isopods, pentastomids, cirripeds), marine helminths (nematodes, acanthocephalans, flukes), gastropod molluscs, insects (ticks, fleas, biting flies, strepispterans), and microsporidia. The period of highest discovery has been most recent for the marine helminths and microsporids. The number of people describing parasites has been increasing since the 1960s, as it has for all other taxa. However, the number of species being described per decade relative to the number of authors has been decreasing except for the helminths. The results indicate that more than half of all parasites have been described, and two-thirds of host taxa, although the proportion varies between taxa. It is highly unlikely that the number of named species of parasites will ever approach that of their hosts. This contrast between the proportion that parasites comprise of local and global faunas suggests that parasites are less host specific and more widespread than local scale studies suggest.