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Consistent patterns of positive selection in functionally similar genes can suggest a common selective pressure across a group of species. We use alignments of orthologous protein-coding genes from 39 species of birds to estimate parameters related to positive selection for 11,000 genes conserved across birds. We show that functional pathways related to the immune system, recombination, lipid metabolism, and phototransduction are enriched for positively selected genes. By comparing our results with mammalian data, we find a significant enrichment for positively selected genes shared between taxa, and that these shared selected genes are enriched for viral immune pathways. Using pathogen-challenge transcriptome data, we show that genes up-regulated in response to pathogens are also enriched for positively selected genes. Together, our results suggest that pathogens, particularly viruses, consistently target the same genes across divergent clades, and that these genes are hotspots of host-pathogen conflict over deep evolutionary time.

Infectious diseases have affected humanity for millennia and are among the strongest selective forces. Tuberculosis (TB) is an ancient disease, caused by the human-adapted members of the Mycobacterium tuberculosis complex (MTBC). The outcome of TB infection and disease is highly variable, and co-evolution between human populations and MTBC strains may account for some of this variability. Particular human genetic ancestries have been associated with higher susceptibility to TB, but sociodemographic aspects of the disease can confound such associations. Here, we studied 1000 TB patients from Dar es Salaam, Tanzania, together with their respective MTBC isolates, by combining human and bacterial genomics with clinical data. We found that the genetic background of the TB patient population was strongly influenced by migrations of Bantu-speaking populations from West Africa, which contrasts with the corresponding MTBC genotypes that were mainly introduced from outside Africa. These findings suggest a recent evolutionary history of co-existence between the human and MTBC populations in Dar es Salaam. We detected no evidence of an effect of human genetic ancestry, or MTBC phylogenetic diversity alone, nor their interaction, on TB disease severity. There was also no evidence of an association between human variation genome-wide and TB disease severity. Treatment-seeking, social, and environmental factors are likely to be the main determinants of disease severity at the point of care in this patient population.

There is increasing evidence that over‐production of reactive species (RS) constitutes a significant physiological cost for migrating birds. The current view entails that RS during migration originate primarily from increased metabolic activity associated with prolonged flights and refueling. In this review, we argue that there is another substantial, yet mostly overlooked, source for RS in migrating birds: infections. Specifically, we highlight that acute and chronic infections during migration are the norm rather than the exception, and that those infections can also result in harmful RS production, either via immune system activation or via the pathogen itself. Thus, infections may impose further oxidative costs on migrating individuals in addition to those directly caused by migratory flights and refueling. Depending on the type of infection and the associated immune responses, these costs may be substantial. Therefore, both migration‐ and infection‐related oxidative challenges should be considered when trying to explain variation in (individual) migration strategies and in coping mechanisms used to mitigate oxidative damage. We explore the ecological and evolutionary consequences of infection during migration in relation to oxidative stress. Specific research on the processes and mechanisms involved in immune‐oxidative stress may lead to fundamental advances in our understanding of the ecology and evolution of migration and residency.

Previous studies suggest overrepresentation of particular polymorphisms within the Helicobacter pylori CagL hypervariable motif (CagLHM) in gastric cancer–associated isolates. However, these disease correlations were geographically variable and ambiguous. We compared the disease correlation of several hundred geographically diverse CagL sequences and identified 33 CagLHM sequence combinations with disparate geographical distribution, revealing substantial worldwide CagLHM diversity, particularly within Asian countries. Notably, polymorphisms E59 and 160 were significantly overrepresented, whereas D58 and E62 were underrepresented, in gastric cancer–associated H. pylori isolates worldwide. Thus, CagLHM regional diversity may contribute to the varied prevalence of H. pylori–related gastric cancer observed in diverse populations.

Background Pathogens can shape their host communities over various timescales. The potential role of host–pathogen co-evolution in driving contemporary shifts in disease ecology is becoming increasingly important as host species emerge and persist outside their native ranges. In North America, Mycoplasma ovipneumoniae can cause fatal pneumonia epizootics in native bighorn sheep ( Ovis canadensis ), whereas introduced free-ranging sympatric aoudad ( Ammotragus lervia ) typically act as asymptomatic reservoirs. We describe the responses of two hosts with different biogeographical histories to shared pathogen exposure through a lens of potential host–pathogen co-evolution. Specifically, this work integrates findings on microbiome composition and host transcriptomic responses in aoudad and bighorn sheep before and after controlled exposure to M. ovipneumoniae , with or without leukotoxigenic Pasteurellaceae. Results Aoudad maintained significantly higher microbial richness (Shannon) in the lower respiratory tract, whereas bighorn sheep experienced post-exposure microbiome perturbations and enhanced growth of some opportunistic taxa. Both molecular detection of and humoral antibodies to M. ovipneumoniae reduced the relative abundance of key genera (e.g., Bibersteinia , Mannheimia , Pasteurella , Roseomonas ) in the upper respiratory tract, but post-exposure bacterial community alteration was more pronounced in bighorn sheep. Transcriptome profiling revealed that, compared to aoudad, bighorn sheep upregulated pro-inflammatory and oxidative-stress pathways—including interleukin-1, interleukin-12, and NF-κB signaling—alongside reactive oxygen species generation. In contrast, aoudad exhibited comparatively muted inflammatory signatures, enhanced expression of molecular chaperones, antigen-processing machinery, and integrin-mediated regulatory genes (notably CD46, ILK, and NFKBIZ). Network analysis identified distinct hub genes likely underpinning effective pathogen clearance and mucosal resilience in aoudad versus immunopathology in bighorn sheep. Conclusions Our integrated microbiome and transcriptomic data underscore the importance of co-evolutionary history in driving host-specific responses to shared respiratory pathogens. Aoudad display microbiome stability and balanced immunoregulation, whereas bighorn sheep suffer dysbiosis and excessive inflammation, potentially increasing mortality risk. Explicit consideration of evolutionary and ecological context regarding host–pathogen co-evolution may increase overall understanding of observed pathobiological and epidemiological patterns commonly targeted for disease management interventions.

Abstract Evolutionary divergence of viruses is most commonly driven by co-divergence with their hosts or through isolation of transmission after host shifts. It remains mostly unknown, however, whether divergent phylogenetic clades within named virus species represent functionally equivalent byproducts of high evolutionary rates or rather incipient virus species. Here, we test these alternatives with genomic data from two widespread phylogenetic clades in Tula orthohantavirus (TULV) within a single evolutionary lineage of their natural rodent host, the common vole Microtus arvalis. We examined voles from forty-two locations in the contact region between clades for TULV infection by reverse transcription (RT)-PCR. Sequencing yielded twenty-three TULV Central North and twenty-one TULV Central South genomes, which differed by 14.9–18.5 per cent at the nucleotide and 2.2–3.7 per cent at the amino acid (AA) level without evidence of recombination or reassortment between clades. Geographic cline analyses demonstrated an abrupt (<1 km wide) transition between the parapatric TULV clades in continuous landscape. This transition was located within the Central mitochondrial lineage of M. arvalis, and genomic single nucleotide polymorphisms showed gradual mixing of host populations across it. Genomic differentiation of hosts was much weaker across the TULV Central North to South transition than across the nearby hybrid zone between two evolutionary lineages in the host. We suggest that these parapatric TULV clades represent functionally distinct, incipient species, which are likely differently affected by genetic polymorphisms in the host. This highlights the potential of natural viral contact zones as systems for investigating the genetic and evolutionary factors enabling or restricting the transmission of RNA viruses.

Malaria persists as a paradigmatic model of co-evolutionary complexity, emerging from the dynamic interplay among a human host, Anopheles vectors, and Plasmodium falciparum parasites. In human populations, centuries of selective pressures have sculpted an intricate and heterogeneous immunogenetic landscape. Classical adaptations, such as hemoglobinopathies, are complemented by a diverse array of genetic polymorphisms that modulate innate and adaptive immune responses. These genetic traits, along with the acquisition of functional immunity following repeated exposures, mitigate disease severity but are continually challenged by the parasite’s highly evolved mechanisms of antigenic variation and immunomodulation. Such host adaptations underscore an evolutionary arms race that perpetually shapes the clinical and epidemiological outcomes. Intermediaries in malaria transmission have evolved robust responses to both natural and anthropogenic pressures. Their vector competence is governed by complex polygenic traits that affect physiological barriers and immune responses during parasite development. Recent studies reveal that these mosquitoes exhibit rapid behavioral and biochemical adaptations, including shifts in host-seeking behavior and the evolution of insecticide resistance. Mechanisms such as enhanced metabolic detoxification and target site insensitivity have emerged in response to the widespread use of insecticides, thereby eroding the efficacy of conventional interventions like insecticide-treated bed nets and indoor residual spraying. These adaptations not only sustain transmission dynamics in intervention saturated landscapes but also challenge current vector control paradigms, necessitating the development of innovative, integrated management strategies. At the molecular level, P. falciparum exemplifies evolutionary ingenuity through extensive genomic streamlining and metabolic reconfiguration. Its compact genome, a result of strategic gene loss and pruning, is optimized for an obligate parasitic lifestyle. The repurposing of the apicoplast for critical anabolic functions including fatty acid, isoprenoid, and haem biosynthesis highlights the parasite’s ability to exploit host derived nutrients efficiently. Moreover, the rapid accumulation of mutations, coupled with an elaborate repertoire for antigenic switching and epigenetic regulation, not only facilitates immune escape but also accelerates the emergence of antimalarial drug resistance. Advanced high throughput sequencing and functional genomics have begun to elucidate the metabolic epigenetic nexus that governs virulence gene expression and antigenic diversity in P. falciparum. By integrating insights from molecular biology, genomics, and evolutionary ecology, this study delineates the multifaceted co-adaptive dynamics that render malaria a recalcitrant global health threat. Our findings provide critical insights into the molecular arms race at the heart of host–pathogen vector interactions and underscore promising avenues for the development of next generation therapeutic and vector management strategies aimed at sustainable malaria elimination.

Ralstonia solanacearum, a species complex of bacterial plant pathogens divided into four monophyletic phylotypes, causes plant diseases in tropical climates around the world. Some strains exhibit a broad host range on solanaceous hosts, while others are highly host-specific as for example some banana-pathogenic strains. Previous studies showed that transcription activator-like (TAL) effectors from Ralstonia, termed RipTALs, are capable of activating reporter genes in planta, if these are preceded by a matching effector binding element (EBE). RipTALs target DNA via their central repeat domain (CRD), where one repeat pairs with one DNA-base of the given EBE. The repeat variable diresidue dictates base repeat specificity in a predictable fashion, known as the TALE code. In this work, we analyze RipTALs across all phylotypes of the Ralstonia solanacearum species complex. We find that RipTALs are prevalent in phylotypes I and IV but absent from most phylotype III and II strains (10/12, 8/14, 1/24, and 1/5 strains contained a RipTAL, respectively). RipTALs originating from strains of the same phylotype show high levels of sequence similarity (>98%) in the N-terminal and C-terminal regions, while RipTALs isolated from different phylotypes show 47-91% sequence similarity in those regions, giving rise to four RipTAL classes. We show that, despite sequence divergence, the base preference for guanine, mediated by the N-terminal region, is conserved across RipTALs of all classes. Using the number and order of repeats found in the CRD, we functionally sub-classify RipTALs, introduce a new simple nomenclature, and predict matching EBEs for all seven distinct RipTALs identified. We experimentally study RipTAL EBEs and uncover that some RipTALs are able to target the EBEs of other RipTALs, referred to as cross-reactivity. In particular, RipTALs from strains with a broad host range on solanaceous hosts cross-react on each other's EBEs. Investigation of sequence divergence between RipTAL repeats allows for a reconstruction of repeat array biogenesis, for example through slipped strand mispairing or gene conversion. Using these studies we show how RipTALs of broad host range strains evolved convergently toward a shared target sequence. Finally, we discuss the differences between TALE-likes of plant pathogens in the context of disease ecology.

If we are to breed common bean (Phaseolus vulgaris L.) for durable resistance to diseases, we must understand pathogenic variation and find sources of resistance. Our first objective was to determine the patterns of pathogenic variation found among isolates of Phaeoisariopsis griseola (PG), the fungus that causes angular leaf spot (ALS) in common bean. We characterized 433 PG isolates from 11 Latin American and 10 African countries, using differential cultivars, isozymes, and/or random amplified polymorphic DNA (RAPD) markers. We also systematically screened, for ALS resistance, common bean accessions from the world collection held at CIAT, and assessed the progress so far made in breeding for resistance to ALS. Despite their great diversity within and between countries on both continents, the PG isolates were classified into two major groups: Andean, and Middle American. Although each group had internal differences for virulence, and biochemical and molecular characteristics, the 'Andean' PG isolates were more virulent on common beans of Andean origin, than on those of Middle American origin, thus, suggesting a host-pathogen co-evolution. The 'Middle American' PG isolates, although more virulent on common beans from Middle America, also attacked Andean beans, thus, exhibiting a much broader virulence spectrum. To find sources of resistance, we tested 22,832 common bean accessions against naturally occurring PG isolates in the field at CIAT's Experiment Station, Quilichao, Colombia, between 1985 and 1992. The resulting 123 intermediate (scores of 4 to 6) and resistant (scores of 1 to 3) accessions were then tested in the greenhouse against selected 14 PG isolates of diverse origins. Nineteen accessions were intermediate or resistant to at least 13 of 14 PG isolates. Similarly, of 13,219 bred lines tested in the field between 1978 and 1996, 89 were intermediate or resistant. Of these, 33 bred lines proved intermediate or resistant to at least eight of nine PG isolates to which they were challenged in the greenhouse. We suggest that, to breed for durable resistance to ALS, common bean populations should be developed from crosses between Andean and Middle American gene pools. The populations should then be systematically evaluated and selected against the broadest range of the most virulent PG isolates of diverse evolutionary origins.[PUBLICATION ABSTRACT]