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Hosts and their symbionts are involved in intimate physiological and ecological interactions. The impact of these interactions on the evolution of each partner depends on the time-scale considered. Short-term dynamics – ‘coevolution’ in the narrow sense – has been reviewed elsewhere. We focus here on the long-term evolutionary dynamics of cospeciation and speciation following host shifts. Whether hosts and their symbionts speciate in parallel, by cospeciation, or through host shifts, is a key issue in host–symbiont evolution. In this review, we first outline approaches to compare divergence between pairwise associated groups of species, their advantages and pitfalls. We then consider recent insights into the long-term evolution of host–parasite and host–mutualist associations by critically reviewing the literature. We show that convincing cases of cospeciation are rare (7%) and that cophylogenetic methods overestimate the occurrence of such events. Finally, we examine the relationships between short-term coevolutionary dynamics and long-term patterns of diversification in host–symbiont associations. We review theoretical and experimental studies showing that short-term dynamics can foster parasite specialization, but that these events can occur following host shifts and do not necessarily involve cospeciation. Overall, there is now substantial evidence to suggest that coevolutionary dynamics of hosts and parasites do not favor long-term cospeciation.

Malaria is one of the most devastating infectious diseases of humans. It is problematic clinically and economically as it prevails in poorer countries and regions, strongly hindering socioeconomic development. The causative agents of malaria are unicellular protozoan parasites belonging to the genus Plasmodium. These parasites infect not only humans but also other vertebrates, from reptiles and birds to mammals. To date, over 200 species of Plasmodium have been formally described, and each species infects a certain range of hosts. Plasmodium species that naturally infect humans and cause malaria in large areas of the world are limited to five— P. falciparum , P. vivax , P. malariae , P. ovale and P. knowlesi . The first four are specific for humans, while P. knowlesi is naturally maintained in macaque monkeys and causes zoonotic malaria widely in South East Asia. Transmission of Plasmodium species between vertebrate hosts depends on an insect vector, which is usually the mosquito. The vector is not just a carrier but the definitive host, where sexual reproduction of Plasmodium species occurs, and the parasite’s development in the insect is essential for transmission to the next vertebrate host. The range of insect species that can support the critical development of Plasmodium depends on the individual parasite species, but all five Plasmodium species causing malaria in humans are transmitted exclusively by anopheline mosquitoes. Plasmodium species have remarkable genetic flexibility which lets them adapt to alterations in the environment, giving them the potential to quickly develop resistance to therapeutics such as antimalarials and to change host specificity. In this article, selected topics involving the Plasmodium species that cause malaria in humans are reviewed.

Both macroclimate and evolutionary events may influence symbiont association and diversity patterns. Here we assess how climatic factors and evolutionary events shape fungal–algal association patterns in the widely distributed lichen-forming fungal genus Protoparmelia. Multilocus phylogenies of fungal and algal partners were generated using 174 specimens. Coalescent-based species delimitation analysis suggested that 23 fungal hosts are associating with 20 algal species. Principal component analysis (PCA) was performed to infer how fungal–algal association patterns varied with climate. Fungi associated with one to three algal partners whereas algae accepted one to five fungal partners. Both fungi and algae were more specific, associating with fewer partners, in the warmer climates. Interaction with more than one partner was more frequent in cooler climates for both the partners. Cophylogenetic analyses suggest congruent fungal–algal phylogenies. Host switch was a more common event in warm climates, whereas failure of the photobiont to diverge with its fungal host was more frequent in cooler climates. We conclude that both environmental factors and evolutionary events drive fungal and algal evolution in Protoparmelia. The processes leading to phylogenetic congruence of fungi and algae are different in different macrohabitats in our study system. Hence, closely related species inhabiting diverse habitats may follow different evolutionary pathways.

Giant viruses are a group of eukaryotic double-stranded DNA viruses with large virion and genome size that challenged the traditional view of virus. Newly isolated strains and sequenced genomes in the last two decades have substantially advanced our knowledge of their host diversity, gene functions, and evolutionary history. Giant viruses are now known to infect hosts from all major supergroups in the eukaryotic tree of life, which predominantly comprises microbial organisms. The seven well-recognized viral clades (taxonomic families) have drastically different host range. Mimiviridae and Phycodnaviridae, both with notable intrafamilial genome variation and high abundance in environmental samples, have members that infect the most diverse eukaryotic lineages. Laboratory experiments and comparative genomics have shed light on the unprecedented functional potential of giant viruses, encoding proteins for genetic information flow, energy metabolism, synthesis of biomolecules, membrane transport, and sensing that allow for sophisticated control of intracellular conditions and cell-environment interactions. Evolutionary genomics can illuminate how current and past hosts shape viral gene repertoires, although it becomes more obscure with divergent sequences and deep phylogenies. Continued works to characterize giant viruses from marine and other environments will further contribute to our understanding of their host range, coding potential, and virus-host coevolution.

Abstract Malaria is considered one of the most important scourges that humanity has faced during its history, being responsible every year for numerous deaths worldwide. The disease is caused by protozoan parasites, among which two species are responsible of the majority of the burden, Plasmodium falciparum and Plasmodium vivax. For these two parasite species, the questions of their origin (how and when they appeared in humans), of their spread throughout the world, as well as how they have adapted to humans have long been of interest to the scientific community. In this paper we review the existing body of knowledge, including current research dealing with these questions, focusing particularly on genetic and genomic analyses of these parasites and comparison with related Plasmodium species infecting other species of host (such as non-human primates). Review of the knowledge obtained from genetic analyses on the origin in humans of Plasmodium falciparum and Plasmodium vivax, the two main agents of human malaria, of their spread throughout the world, as well as how they have adapted to our species.

Every human suffers through life a number of papillomaviruses (PVs) infections, most of them asymptomatic. A notable exception are persistent infections by Human papillomavirus 16 (HPV16), the most oncogenic infectious agent for humans and responsible for most infection-driven anogenital cancers. Oncogenic potential is not homogeneous among HPV16 lineages, and genetic variation within HPV16 exhibits some geographic structure. However, an in-depth analysis of the HPV16 evolutionary history was still wanting. We have analyzed extant HPV16 diversity and compared the evolutionary and phylogeographical patterns of humans and of HPV16. We show that codivergence with modern humans explains at most 30% of the present viral geographical distribution. The most explanatory scenario suggests that ancestral HPV16 already infected ancestral human populations and that viral lineages co-diverged with the hosts in parallel with the split between archaic Neanderthal-Denisovans and ancestral modern human populations, generating the ancestral HPV16A and HPV16BCD viral lineages, respectively. We propose that after out-of-Africa migration of modern human ancestors, sexual transmission between human populations introduced HPV16A into modern human ancestor populations. We hypothesize that differential coevolution of HPV16 lineages with different but closely related ancestral human populations and subsequent host-switch events in parallel with introgression of archaic alleles into the genomes of modern human ancestors may be largely responsible for the present-day differential prevalence and association with cancers for HPV16 variants.

1. Emerging infectious diseases (EIDs) are recognized as having significant social, economic and ecological costs, threatening human health, food security, wildlife conservation and biodiversity. We review the processes underlying the emergence of infectious disease, focusing on the similarities and differences between conceptual models of disease emergence and biological invasions in general. 2. Study of the IUCN's list of the world's worst invaders reveals that disease is cited as a driver behind the conservation, medical or economic impact of nearly a quarter of the species on the data base. 3. The emergence of novel diseases in new host species are, in essence, examples of invasions by parasites. Many of the ecological and anthropogenic drivers of disease emergence and classical invasions are also shared, with environmental change and global transport providing opportunities for the introduction and spread of invaders and novel parasites. 4. The phases of disease emergence and biological invasions have many parallels; particularly the early and late phases, where demographic and anthropogenic factors are key drivers. However, there are also differences in the intermediate phases, where host—parasite co-evolution plays a crucial role in determining parasite establishment in novel hosts. 5. Similar opportunities and constraints on control and management occur at the different phases of invasions and disease emergence. However, exploitation of host immune responses offers additional control opportunities through contact control and vaccination against EIDs. We propose that cross-fertilization between the disciplines of disease emergence and invasion biology may provide further insights into their prediction, control and management.

Species of Cryphonectriaceae can occur as asymptomatic fungal endophytes in Melastomataceae trees and shrubs. One hypothesis suggests Chrysoporthe cubensis (Cryphonectriaceae) is an endophyte of the Melastomataceae that has undergone a host switch to infect species of Eucalyptus in South America. The potential for similar host switches by other species of the Cryphonectriaceae is exacerbated by native stands of Melastomataceae that grow alongside commercial plantations of Eucalyptus. We sought to determine the diversity of Cryphonectriaceae endophytic in Melastomataceae trees that occur naturally adjacent to Eucalyptus plantations in Colombia. Branch segments were taken from six different species in three genera of the Melastomataceae. A technique that simulated natural conditions was used to promote fruiting of endophytic Cryphonectriaceae. Taxa were identified using a phylogenetic species concept based on sequence data from the internal transcribed spacer and β-tubulin gene regions. Three species of Cryphonectriaceae, Aurapex penicillata, C. cubensis and C. inopina, were identified. We tested whether these endophytes were potential pathogens of Eucalyptus, and each species was mildly pathogenic. The results showed that at least six species of Melastomataceae are hosts of the Cryphonectriaceae in Colombia. They also emphasize the biosecurity risk of moving superficially healthy stem tissue of the Melastomataceae to new environments.

Central to the concept of ecological speciation is the evolution of ecotypes, i.e. groups of individuals occupying different ecological niches. However, the mechanisms behind the first step of separation, the switch of individuals into new niches, are unclear. One long-standing hypothesis, which was proposed for insects but never tested, is that early learning causes new ecological preferences, leading to a switch into a new niche within one generation. Here, we show that a host switch occurred within a parasitoid wasp, which is associated with the ability for early learning and the splitting into separate lineages during speciation. Lariophagus distinguendus consists of two genetically distinct lineages, most likely representing different species. One attacks drugstore beetle larvae (Stegobium paniceum (L.)), which were probably the ancestral host of both lineages. The drugstore beetle lineage has an innate host preference that cannot be altered by experience. In contrast, the second lineage is found on Sitophilus weevils as hosts and changes its preference by early learning. We conclude that a host switch has occurred in the ancestor of the second lineage, which must have been enabled by early learning. Because early learning is widespread in insects, it might have facilitated ecological divergence and associated speciation in this hyperdiverse group.

In natural ecosystems, parasites often infect multiple host species, particularly when hosts share habitats, facilitating host-to-host transmission and altering traditional host-parasite coevolution dynamics. This study examines the microsporidian parasite Nosema ceranae in Eastern honey bees ( Apis cerana ) and Western honey bees ( Apis mellifera ), assessing its virulence and proliferation dynamics. Using inoculation experiments, we measured bee mortality and parasite spore loads to infer virulence and proliferation. Additionally, time-series transcriptome analysis of both bees and parasites provide insights into host-pathogen interactions. The results reveal that N. ceranae produces more spores with lower mortality in A. mellifera but causes higher mortality with lower spore production in A. cerana . The parasite also suppresses host gene expression, with stronger suppression observed in A. cerana . These findings suggest that N. ceranae is adapted for low virulence and high proliferation in A. mellifera but exhibits high virulence and limited proliferation in A. cerana . This study highlights the evolution of distinct trade-offs between virulence and proliferation in a multi-host system, offering valuable insights into parasite-host dynamics and their ecological implications.