Dengue virus (DENV), a major arboviral pathogen of global concern, evolves rapidly through a combination of intrinsic molecular mechanisms, vector adaptation, and host immune pressures. Despite extensive research, major gap remains in understanding how these forces, collectively generate, shape, and fix adaptive mutations that drive DENV evolution. In this review, we explore the molecular mechanisms underlying DENV evolution, with emphasising the error-prone RNA-dependent RNA polymerase, template switching, recombination, and the modulatory effects of viral RNA secondary structures. We also highlight the replicase complex's intrinsic tolerance to mutations as a driver of evolutionary plasticity. At the protein level, we summarise adaptive mutation in capsid, envelop, NS1 and NS5 protein that influence virulence, transmission efficiency, and immune escape. Additionally, we also address the role of vector adaptation, whereby DENV overcomes midgut and salivary gland infection barriers in Aedes mosquitoes, often through bottleneck-driven selection and compensatory mutations, consequently enhancing transmission potential. Finally, we discuss host immune-driven selection including T cell-mediated immune responses, and the regulation of IFN, NF-κB, and PI3K/Akt/mTOR signalling pathways shapes the evolution of DENV. Together, these insights highlight the dynamic interplay between viral genetics, mosquito vectors, and host immunity in shaping the evolutionary trajectory of DENV.

This paper proposes a physics-informed global path planning framework for underwater vehicles integrating CFD simulation and the genetic algorithm. The CFD simulation models the flow field along the planned path of the underwater vehicle. The current velocity data are incorporated into the following path planning that is based on an improved genetic algorithm (GA), which uses migration operators to share the information about feasible solutions or paths, improving the fitness of the whole population. In the three steps of the GA procedure, an elite selection strategy is adopted to avoid losing excellent solutions. A segmented crossover strategy is adopted to avoid low-quality crossover. An adaptive mutation strategy is used to enhance the ability to escape a local optimal solution. Using the improved GA, single-target and multi-target underwater path planning are investigated. In multi-target path planning, a combined algorithm is proposed to solve the optimal traversal order of target points and plan a feasible path between target points. The simulation results show that the proposed algorithm has good planning ability for both simple and complex underwater scenarios. Compared with the conventional GA and an improved GA, the number of average iterations decreases by 45.3% and 29.9%, respectively, for 2D multi-target path planning. The number of average inflection points decreases by 50.3% and 44.2%, respectively, for 2D multi-target path planning.

To investigate the molecular characteristics of H3N2 canine influenza viruses circulating in Jiangsu, China, we isolated a H3N2 strain (A/Canine/Nanjing/CnNj01-2025) from a dog presenting with respiratory signs at the Veterinary Teaching Hospital of Nanjing Agricultural University. All eight gene segments were sequenced and compared with those of two human H3N2 strains and five avian H3N2 strains. Antigenicity and receptor-binding properties were also assessed. Phylogenetic analysis revealed that the canine isolate descended from the avian lineage and formed an independent evolutionary clade, while the human strains were more distantly related to the avian lineage. Glycosylation analysis of the HA protein revealed that the canine strain carried seven N-glycosylation sites, including a unique site at residue 97/81 (HA/H3 numbering), which serves as a molecular signature of the canine strain. Several amino-acid substitutions were identified in major antigenic sites, including D97/81N, A176/160T, N204/188D, V212/196I, and W237/222L. Analysis of internal genes showed that the canine strain harbored PB2 292T and 590S mammalian adaptation mutations, which are also present in human strains. Hemagglutination inhibition (HI) assays of the canine strain indicated moderate serologic cross-reactivity with a human H3N2 antiserum (16-fold reduction), whereas avian strains showed no cross-reactivity. Receptor-binding assays demonstrated that the virus retained predominant α-2,3 sialic acid binding, comparable to that of avian influenza viruses, and gained a modest affinity for human-type α-2,6 sialic acid receptors. Therefore, the canine H3N2 virus has undergone significant antigenic drift, developed partial serological cross-reactivity with human strains, and acquired detectable but limited binding affinity for human-type receptors. Overall, our findings suggest that the current canine H3N2 influenza virus exhibits distinct genetic and antigenic variations from human and avian strains. Continuous molecular and serological surveillance of canine influenza viruses is therefore warranted to monitor their evolutionary trends and assess the potential for cross-species transmission.

The forces driving virus evolution are central to understanding cross-species transmission and virus emergence. It is well established that the adaptive immune system drives virus evolution in mammals, but whether innate responses likewise drive virus evolution upon host shifts is less well understood. In this manuscript, we used Drosophila melanogaster as a model to study the evolution of a native and a nonnative pathogen under conditions in which innate antiviral immunity is either abolished or enhanced. Using an experimental evolution approach, we find little evidence for adaptive evolution of the natural pathogen Drosophila C virus. In contrast, we observed a recurrent adaptive mutation in the viral nonstructural 2B protein in the nonnative cricket paralysis virus, independent of the antiviral cGAS/STING pathway. Our work provides insights into viral adaptation to new hosts and the characteristics of the 2B protein of dicistroviruses, a family comprising important model insect viruses.

Highly pathogenic avian influenza H5N1 poses an increasing public health risk, particularly following its spillover into dairy cows and associated human infections in the U.S. since March 2024. Here, we systematically identified critical PB2 mutations emerged during avian-to-cattle transmission and subsequent adaptation in cattle, notably PB2 M631L, which conferred pathogenicity in mice comparable to the well-characterized PB2 E627K mutation. Retrospective analysis reveals that PB2 631L also circulated in avian and human H5N1 strains during the 2013-2014 outbreaks in Cambodia and Vietnam. Additional adaptive mutations include established markers (E627K, Q591R, D701N), and novel variants (I647V, G685R, K736R). These mutations enhance polymerase activity by improving the utilization of both bovine and human ANP32A proteins, thereby increasing viral fitness and pathogenicity in mammals. The convergence of these adaptations highlights the elevated zoonotic risk of cattle-adapted H5N1 viruses and underscores the urgent need for heightened surveillance across avian and mammalian hosts.

Bradyrhizobium and Sinorhizobium are dominant soybean microsymbionts in acidic/neutral and alkaline soils, respectively. However, the molecular mechanisms underlying this pH-dependent adaptation remain elusive. In this study, phylogenomic analysis of 286 Bradyrhizobium and 322 Sinorhizobium genomes revealed that Bradyrhizobium possesses abundant xeno-siderophore receptors but has limited siderophore biosynthesis functions. In contrast, gene clusters directing siderophore biosynthesis are enriched in Sinorhizobium. As siderophores can chelate the prevalent insoluble Fe3+ under neutral and alkaline conditions, whereas being less important in acidic environments where soluble Fe2+ is readily accessible, we hypothesized that the genus-dependent phyletic distribution of siderophore biosynthesis and exploitation functions may contribute to the pH adaptation of these two genera. Indeed, Bradyrhizobium species barely grow under iron-limiting conditions, and this growth defect can be rescued by xeno-siderophores produced by Sinorhizobium. Using a xeno-siderophore-exploiting Bradyrhizobium diazoefficiens strain, an engineered xeno-siderophore exploiter, and an altruistic siderophore-producing strain derived from Sinorhizobium fredii, we revealed the competitive advantage of xeno-siderophore exploitation during soybean nodulation. Heterologous expression of certain Bradyrhizobium xeno-siderophore receptors, along with various adaptive mutations in the genome of the S. fredii receptor-lacking mutant, allowed this mutant to rapidly restore growth under iron-limiting conditions. These adaptive events in experimental evolution depend on the siderophore biosynthetic function of S. fredii. Taken together, these findings suggest that the siderophore utilization ability of soybean rhizobia can be positively selected under iron-limiting conditions: by maintaining abundant xeno-siderophore receptors in acid-tolerant Bradyrhizobium and by the rapid adaptive evolution of utilization machinery for self-produced siderophores in alkaline-tolerant Sinorhizobium.

Chikungunya fever (CHIKF) is a re-emerging mosquito-borne viral disease with an expanding global and regional footprint. This study investigates its epidemiological trends, molecular evolution, and control strategies, with a particular focus on recent developments in China. Drawing on data from 2010–2025, it integrates spatial, temporal, and genomic analyses to elucidate transmission dynamics and adaptive mutations. Globally, cyclical outbreaks occur every 3–5 years, driven primarily by the East/Central/South African (ECSA) lineage’s enhanced transmissibility via Aedes albopictus. In China, chikungunya has progressed from sporadic importations to limited local circulation, especially in Guangdong and Fujian provinces. Molecular evidence reveals ECSA-derived variants carrying adaptive mutations (E1:A226V, E2:L210Q) that confer improved vector adaptation. Persistent challenges—including misdiagnosis, fragmented surveillance systems, and inconsistent genomic monitoring—continue to hinder effective control. This study highlights the urgent need for integrated vector management, strengthened molecular surveillance, and regional cooperation to prevent endemic establishment and reduce chikungunya’s long-term public health and socioeconomic impacts.

SARS-CoV-2 rapidly adapts to new hosts following cross-species transmission; this is highly relevant as unique within-host variants have emerged following infection of susceptible wild and domestic animal species. Furthermore, SARS-CoV-2 transmission from animals (e.g., white-tailed deer, mink, domestic cats, and others) back to humans has been observed, documenting the potential of animal-derived variants to infect humans. Here, we investigate SARS-CoV-2 evolution and host-specific adaptation during an outbreak in Amur tigers (Panthera tigris altaica), African lions (Panthera leo), and spotted hyenas (Crocuta crocuta) at Denver Zoo in 2021. SARS-CoV-2 genomes from longitudinal samples from 16 individuals are evaluated for within-host variation and genomic signatures of selection, and we determine that the outbreak was likely initiated by a single spillover of a rare Delta sublineage. Within-host virus populations rapidly expand and diversify, and we detect signatures of purifying and positive selection, including strong positive selection in hyenas and in the nucleocapsid (N) gene in all animals. Four candidate species-specific adaptive mutations are identified: N A254V in lions and hyenas, and ORF1a E1724D, spike T274I, and N P326L in hyenas. These results reveal accelerated SARS-CoV-2 adaptation following host shifts in three non-domestic species in daily contact with humans.

Microorganisms rapidly adapt to non-lethal stress through mutations, a process central to microbial evolution. In this study, we investigate the molecular mechanism of adaptive mutagenesis in the bacterial strain Escherichia coli K-12 harboring a frameshift lac mutation. A non-random mutational spectrum, featuring a prominent - 1bp deletion hot-spot is an intriguing unsolved phenomenon seen in the revertants of starving cells of this strain. The very-short-patch mismatch repair, a stationary-phase specific DNA repair pathway, has been hypothesized to create this hot-spot. To test this, we independently inactivated two main players of this pathway: dcm involved in DNA cytosine methylation and vsr encoding a sequence-specific DNA repair endonuclease. Contrary to the prediction of our hypothesis, the stationary-phase mutational spectra of Δdcm and Δvsr strains were indistinguishable from that of the wild-type strain, i.e., the frequency of mutations at the hot-spot remained unchanged. Unexpectedly, both Δdcm and Δvsr strains showed a two-fold increase in stationary-phase reversion frequency with respect to the wild-type strain. This result differed from an earlier finding where simultaneous deletion of both genes had no effect. We conclude that the adaptive mutation hot-spot is not caused by very-short-patch mismatch repair. Instead, our data suggest that dcm and vsr independently influence adaptive mutagenesis rate, possibly through previously unrecognized 'moonlighting' functions. Future work will aim to uncover the mechanism behind this unique adaptive mutational spectrum, advancing our understanding of stress-induced mutagenesis.

Cell volume, a key determinant of physiology, is maintained by cell size homeostasis. Large deviations from typical size are often harmful, yet cell sizes have diverged drastically in evolution. How does size homeostasis evolve to support such diversity without impairing physiology? To address this, we used experimental evolution to select progressively smaller Saccharomyces cerevisiae cells. Over 1,500 generations, we achieved a six-fold volume reduction compared to wild type. Size homeostasis remained robust and evolutionary stable, with cells maintaining competitive fitness, indicating that dramatic volume changes need not compromise physiology. We investigated the genetic basis of cellular miniaturization through whole-genome sequencing of the evolving populations. We show that genetic manipulations of the G1 cyclin CLN3 and the Greatwall kinase RIM15 signaling cascades produce a fourteen-fold change in cell size, with adaptive mutations recapitulating the evolved volumes and loss-of-function mutations yielding enlarged cells. Our results demonstrate the evolutionary plasticity of cell size homeostasis and reveal a mechanism for eukaryotic cell size evolution.

Objective: To conduct a molecular epidemiological investigation and genetic characteristics of the local outbreak of Chikungunya fever in Guangzhou City in July 2025, clarify the source, genotype, and variation characteristics of the virus, and provide a scientific basis for traceability and prevention and control of the outbreak. Method: Epidemiological data and serum samples of confirmed cases were collected. The virus nucleic acid testing, whole genome sequencing, phylogenetic tree reconstruction, and E1/E2 protein amino acid site analysis were performed. Results: By August 6, 2025, 104 autochthonous Chikungunya cases had been confirmed in Guangzhou City, showing a spatially scattered transmission pattern with limited cluster potential in areas such as Xintang Town. Fifty-one full-genome sequences were obtained, all belonging to the East/Central/South African (ECSA) genotype, Central African subclade, with a similarity of 99.96% to the Réunion Island strains (2024-2025). Fifteen amino acid mutations were identified in E1/E2 proteins, of which 13 were unique, including adaptive mutations such as E1-A226V and E2-I211T. Conclusion: The outbreak is caused by a single imported ECSA-genotype strain, potentially from the Indian Ocean region. There may be a risk of small-scale outbreaks in Guangzhou City. Continuously strengthening mosquito-borne disease surveillance, early warning systems, and etiological monitoring is significant for disease prevention and control.

Increase in human H5N1 spillover infections resulting from dissemination of highly pathogenic avian influenza (HPAI) virus into bird and mammal populations raises concerns about HPAI gaining human transmissibility. Studies identified hemagglutinin (HA) acid stability and receptor preference as essential traits that shape host tropism. Mutations that increase HA stability and affinity for α−2,6-linked sialic acids have been shown to confer airborne transmissibility in a ferret model, however mechanisms of activation of H5 subtype HA are poorly understood and the effect of adaptive mutations on HA function has been largely inferred from static structures. Here, we use hydrogen/deuterium-exchange mass spectrometry to dissect activation dynamics for two ancestral H5 HPAI HA, their transmission-adapted HA, and a contemporary HA. We identify variation in receptor binding site flexibility and demonstrate that adaptive mutations result in suppression of fusion peptide dynamics and stabilization of a key interface involved in activation. The contemporary H5 isolated from a spillover event exhibits a relatively protected fusion peptide and moderately depressed activation pH compared to ancestral HAs. Our studies of activation dynamics in H5 together with analysis of H1 and H3 HAs reveal subtype-specific patterns that correlate with mutation sites and indicate underlying physical constraints on influenza HA adaptation.

The circulating strain in the recent Chikungunya fever outbreak in Guangdong Province belongs to the East/Central/South African (ECSA) genotype. However, the specific mutations in the viral genome remained unclear. This study conducted whole-genome sequencing of viral sequences from clinical samples. The results confirmed that the epidemic strain belongs to the Middle African Lineage (MAL) within the ECSA genotype, not the Indian Ocean Lineage (IOL). Further analysis of nucleotide mutations revealed several adaptive mutations compared with the S27 genomic sequence (NC_004162), such as E1-A226V, E2-L210Q, and E2-I211T. Based on previous genomic surveillance and pathogen studies, mutations like E1-A226V, E2-L210Q, and E2-I211T were generally considered characteristic of IOL within the ECSA genotype and are known to enhance viral replication and transmission efficiency in Aedes albopictus mosquitoes. This study identifies the circulating strain in Guangdong belongs to MAL, which is phylogenetically distinct from IOL, yet also carries these mutations. This suggests these may represent adaptive changes in the MAL strain to a new mosquito host. In Guangdong Province, Ae. albopictus is the predominant mosquito species, while the distribution of Ae. aegypti is relatively limited. The ecological predominance of Ae. albopictus likely serves as a key contributing factor facilitating the rapid importation and subsequent widespread dissemination of the current epidemic strain.

Guanidine is well known as a denaturing agent. However, recent studies have demonstrated both the widespread synthesis of guanidine, e.g., in plants and mammals, as well as the widespread occurrence of guanidine metabolism in bacteria, suggesting a broader biological role. Here, we provide insights into guanidine assimilation via guanidine hydrolases (GdmH) in cyanobacteria. The gdmH gene is widespread among cyanobacteria and enables growth on guanidine as the sole nitrogen source. Consistent with this, gdmH gene expression increased under nitrogen limitation, regulated by the transcription factor NtcA. However, guanidine is toxic above 5 mM, necessitating GdmH activity and adaptive mutations activating the multidrug efflux system PrqA. The gdmH gene is frequently colocalized with ABC transporter genes (named gimABC), which are driven by an additional NtcA-regulated promoter. The corresponding substrate-binding protein GimA showed high affinity to guanidine. Consistent with a high affinity import system, disruption of genes gimA or gimB impaired guanidine-dependent growth of Synechocystis sp. PCC 6803 at low concentrations. However, in presence of >1 mM guanidine, these mutants grew like wildtype, suggesting the existence of additional uptake mechanisms for guanidine. We also demonstrate the high-affinity binding of guanidine to a previously described, conserved RNA motif located within the gdmH 5'-untranslated region, validating it as a guanidine-I riboswitch. By combining it with various promoters, we achieved precise, titratable control of heterologous gene expression in cyanobacteria in vivo. Our findings establish guanidine assimilation as an integral element of cyanobacterial nitrogen metabolism and highlight guanidine riboswitches as valuable tools for synthetic biology.

Metaheuristic high utility itemsets mining algorithms often face challenges such as poor initial population quality, low time efficiency, and itemsets loss due to premature convergence. To address these issues, this study proposes a high utility itemsets mining algorithm based on co-evolution. A population initialization strategy based on logarithmic decay and probability distribution is proposed to enhance population diversity and improve the quality of initial solutions. Additionally, to improve search efficiency and computational performance, a co-evolutionary update strategy is designed, where particle swarm optimization enhances the Lévy flight mechanism in cuckoo search. Furthermore, an adaptive simplified mutation strategy is introduced to increase population diversity and convergence speed, thereby reducing the risk of itemset loss. Experimental results show that the proposed algorithm outperforms state-of-the-art methods in terms of the number of high utility itemsets mined, runtime, recall, precision, and convergence.

Humans and microbes: A systems theory perspective on coevolution.

The cross-species transmission of avian H9N2 influenza viruses to swine increases the risk of viral adaptation to mammalian hosts. However, the mechanisms by which these H9 viruses can overcome the barriers posed by swine hosts have not yet been fully elucidated. In previous studies, we identified avian H9 strains exhibiting either infective or noninfective phenotypes in swine. Here, we investigated the role of surface genes in cross-species transmission by replacing the surface genes of noninfective strains with those of their infective counterparts. We demonstrated that the surface genes of the infective strains, particularly the hemagglutinin (HA) gene, restored infectivity in pigs for two previously noninfective strains. Surface genes from infective strains significantly increased viral replication efficiency in both CEF and PK15 cells, and recombinant viruses carrying these genes presented superior thermal stability. Amino acid sequence analysis of HA identified six critical residues (30T, 39A, 327R, 373K, 465K, and 490R) associated with infectivity in pigs. Avian H9 viruses bearing these swine-adaptive molecular signatures began emerging in terrestrial poultry before the 2000s and subsequently achieved dominance through widespread dissemination. These findings suggest that molecular changes in HA accumulated during the adaptation of avian H9 viruses in terrestrial poultry may drive the emergence of swine-infective strains. This study elucidates key molecular determinants that enable avian H9 viruses to infect swine and highlights the public health implications of prolonged H9N2 circulation in terrestrial poultry, which facilitates mammalian adaptation. These insights underscore the need for intensified surveillance of avian-to-swine influenza transmission dynamics.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13567-025-01678-7.

ABSTRACT Chikungunya virus (CHIKV) caused more than 10,000 infections in Foshan, Guangdong, in 2025. Using plasma from acute-phase patients, we successfully isolated infectious CHIKV, confirmed by focus-forming assay and transmission electron microscopy. Whole-genome sequencing revealed that all isolates belonged to the ECSA-2 sub-lineage and were closely related to strains circulating on Réunion Island in 2024–2025, carrying adaptive mutations including C:T143A, E1:A226 V, and E2:I211 T/L210Q. Based on Foshan’s 2025 population (∼9.6 million), the outbreak corresponded to a cumulative incidence of ∼104 cases per 100,000 inhabitants, highlighting intense transmission. Integrated virological, genomic, and epidemiological analyses characterize the rapid expansion of a single ECSA-2 genotype and underscore the need for strengthened arbovirus and genomic surveillance in southern China.

Achieving high operational efficiency in modern manufacturing requires the seamless integration of production scheduling and intralogistics coordination. However, in flexible assembly shops, the decoupling between production sequencing and automated guided vehicle (AGV) routing often leads to resource conflicts, unbalanced workloads, and inefficient energy utilization. To address this challenge, this study proposes an improved genetic algorithm (IGA) for integrated production–logistics scheduling. The innovation lies in a triple-chain encoding strategy that concurrently represents production, transportation, and time-window constraints, coupled with adaptive crossover and mutation operators for enhanced population diversity. Furthermore, a time-window-constrained Dijkstra routing mechanism is incorporated to prevent AGV conflicts and improve synchronization between machines and logistics. Two representative shop-floor scenarios—baseline and disturbed conditions—were designed for validation. Comparative experiments against a standard genetic algorithm (GA) and a two-stage heuristic demonstrate that the IGA achieves 9.5% and 6.7% reductions in average makespan, respectively, while maintaining less than 1% deviation under 10% random disturbances. Statistical tests (p < 0.01, Cohen’s d > 1.4) confirm the method’s robustness and practical effectiveness. The proposed approach provides a reliable and implementable optimization framework that enhances coordination between production and AGV systems in flexible assembly environments and offers a practical reference for smart manufacturing scheduling and digital twin applications.

To address the problems of low identification accuracy, poor global search capability, and susceptibility to local optima in permanent magnet synchronous motor (PMSM) parameter identification, this paper proposes a hybrid niching clonal selection black widow optimization (NCS-BWO) algorithm. This algorithm combines the exploitation capability of black widow optimization (BWO) with the exploration capability of the clonal selection algorithm (CSA). First, a niching strategy called nearest-better clustering (NBC) is used to generate sub-populations, incorporating a cluster size optimization mechanism to ensure a balanced population distribution. Subsequently, adaptive Gaussian mutation and elite differential evolution (DE) mutation operators are introduced during the CSA hypermutation stage. Finally, the high-quality population resulting from the niching clonal selection algorithm (NCSA) serves as the initial population for the BWO. The effectiveness of the NCS-BWO algorithm was validated using six benchmark test functions, and its performance was compared with that of six other algorithms. Furthermore, a full-rank discrete model of the PMSM was established, and the NCS-BWO algorithm was applied for parameter identification. Both the simulation and experimental results demonstrate that the proposed NCS-BWO algorithm achieves superior accuracy in PMSM parameter identification.