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PubMed2026

Cryo-EM structure, enzymatic activity and genome targeting of canonical PRC1.

Canonical Polycomb repressive complex 1 (cPRC1) preserves cell fate decisions by repressing aberrant transcription of developmental regulator genes. We report the cryo-electron microscopy structure of the human cPRC1 holocomplex assembled from RING1B, BMI1, PHC2 and CBX7 bound to an H3K27me3-modified mononucleosome together with the ubiquitin-conjugating enzyme UBCH5C. cPRC1 adopts a compact, highly integrated architecture in which the subunits RING1B, BMI1 and PHC2 form an extended interface that positions UBCH5C on the nucleosome to enable efficient monoubiquitination of histone H2A at K119. This organization is conserved in Drosophila, where mutational analyses identify the PHC2 ortholog Polyhomeotic (Ph) as a central scaffold and targeting factor. The Ph HD domain is required for complex assembly, whereas the Ph SAM domain is dispensable for assembly but essential for cPRC1 recruitment to Polycomb target genes and productive H2A monoubiquitination at these loci.

Journal Article↗

PubMed2026

Uncovering the genomic landscape of Mycobacterium bovis in Wales.

Bovine tuberculosis (bTB), caused by the bacterium Mycobacterium bovis, is one of the most pressing animal health issues in Wales today. It negatively impacts cattle health, affects profitability and trade, and can decimate years of genetic improvement towards desirable production traits. It also imposes substantial financial, social, and psychological burdens on farming communities. Eradication of bTB requires an understanding of local transmission pathways to target effective disease-control interventions. In this study, we characterised the genomic diversity of M. bovis across Wales by analysing the genome sequence of 379 M. bovis isolates obtained from culture-positive animals in Wales in 2021. Analyses uncovered three prevalent clusters that are geographically distinct. A further three clusters containing fewer isolates were also geographically separated, two of which had particularly large SNP distances from most other Welsh isolates, suggesting independent introductions of M. bovis strains that are not endemic to Wales. Fine-scale and epidemiologically relevant genetic structuring was identified within the six main clusters, indicating region-specific evolution, which can drive local disease dynamics. Finally, SNPs were identified in coding genes that have the potential for important advantageous physiological consequences that may impact host-pathogen interactions and necessitate further investigation.

Animals↗

PubMed2026

Cell cycle-dependent protein dynamics in budding yeast resolved by deconvolution of bulk proteomics.

The cell division cycle is characterised by oscillatory dynamics in regulatory mechanisms and biosynthesis, coordinated with genome replication and segregation. To understand these dynamics, quantitative cell cycle-dependent protein concentration data are essential. Unfortunately, accurately resolving cell cycle-dependent protein dynamics is challenging because single-cell proteomics is currently infeasible and bulk proteomics requires - inherently imperfect - cell synchronisation. Here, we developed a computational method to deconvolve cell cycle-dependent protein concentration dynamics and applied it to new budding yeast bulk proteome data. Key to this method was a yeast population model, parameterised with experimental cell cycle progression and volume growth data, for quantifying the desynchronisation in sampled populations. We performed deconvolution on 3272 proteins, using cross-validation to determine regularisation parameters, and identified 539 proteins with cell cycle-dependent dynamics. Many of these dynamics were consistent with known yeast biology and dynamic proteins were enriched for several metabolic process, extending previous observations and supporting the emerging picture of metabolic activity as varying substantially over cell cycle phases. We consider the generated cell cycle-resolved budding yeast proteome data a key resource.

Journal Article↗

PubMed2026

[Sex-specific depression risk].

Major depression displays significant heritability, and its genetic background has been extensively explored by genome-wide association studies. On the whole, these results indicate a highly polygenic landscape with significant sex-linked differences revealing a higher and more polygenic genetic influence in females than in males.

Humans↗

PubMed2026

[Syphilis and human treponemes: a long evolutionary history revealed by paleogenomics].

Recent discoveries in paleogenomics have revolutionized our understanding of syphilis and other human treponematoses. Far from being a pathogen that suddenly appeared in Europe in the late Middle Ages, we now know that Treponema pallidum has been circulated among human populations for millennia. Ancient genomes recovered from pre-Columbian contexts in the Americas show that major treponemal lineages had already diversified well before the modern era, often in the absence of recognizable skeletal lesions. Genomic analyses further indicate that treponemal diversity is not the result of extensive genetic acquisition, but rather of small-scale modulation of a highly conserved genome, notably via antigenic variation involving the tpr gene family. Combined with data on endemic treponematoses, congenital syphilis, and historical pathology collections, these findings support a model in which syphilis, yaws, and bejel represent context-dependent expressions of an ancient treponemal continuum, with implications for diagnosis, epidemiology, and vaccine design.

Humans↗

PubMed2026

Looking to the Future: How Will Personalised Medicine Impact Facial Plastic Surgery.

AIMS AND BACKGROUNDS: The objectives of this study are to examine the emerging role of personalized medicine in facial plastic surgery and to consider how biologically, anatomically, and psychologically tailored approaches may refine both aesthetic and reconstructive care. HISTORICAL ASPECTS: Facial plastic surgery has traditionally relied on anatomical principles, surgical expertise, and population-based evidence. Personalized medicine represents a shift toward more individualized care by incorporating patient-specific biological and phenotypic variation into clinical decision-making. ANATOMY: Facial plastic surgery is uniquely dependent on subtle anatomical variation, soft tissue characteristics, wound healing behavior, and age-related change. These factors differ considerably between individuals and have a direct impact on both surgical planning and outcomes. TECHNOLOGY: Advances in genomics, pharmacogenomics, artificial intelligence, tissue engineering, and three-dimensional modelling are expanding the scope of personalized care. These technologies may improve prediction of healing, treatment response, complication risk, and reconstructive requirements. PATIENT SELECTION: Personalized medicine may support more accurate patient selection by identifying those at increased risk of adverse scarring, variable response to injectables or pharmacotherapy, or differential reconstructive needs, thereby improving counselling and expectation management. TECHNIQUES: Potential applications include tailored incision planning, individualized facial rejuvenation strategies, personalized perioperative pharmacological regimens, and patient-specific reconstructive scaffolds, grafts, and implants. POSTOPERATIVE CARE: Postoperative management may also become more individualized through better prediction of inflammatory response, scar formation, analgesic requirements, and recovery trajectory, allowing more precise surveillance and adjunctive treatment. CURRENT AND FUTURE DEVELOPMENT: Although many applications remain investigational, continued progress in regenerative medicine, molecular profiling, and predictive analytics is likely to accelerate clinical translation. Ethical challenges relating to privacy, bias, and equitable access must, however, remain central. CONCLUSION AND CLINICAL RELEVANCE: Personalized medicine has the potential to enhance precision, safety, and patient-centered care in facial plastic surgery. Its future value will depend on thoughtful integration into practice as an adjunct to, rather than a replacement for, surgical judgement and aesthetic insight.

Journal Article↗

PubMed2026

Intestinal plasmacytoid dendritic cells preferentially produce interferon lambda, contributing to localized innate immune responses.

The healthy intestine maintains homeostasis in part via immune responses to microbiota, which includes basal production of interferon cytokines. Previous work showed that Type III Interferon (IFN-λ) stimulates localized pockets of interferon-stimulated genes (ISGs) in the adult mouse intestinal epithelium at homeostasis that provide preemptive protection from viral pathogens. Here, we demonstrate that a major source of homeostatic IFN-λ production in the intestine is a population of epithelium-associated plasmacytoid dendritic cells (pDC). Expansion of the pDC population increases epithelial ISG expression at homeostasis, suggesting the abundance of these cells is a limiting factor in IFN-λ responses. On the other hand, depletion of pDC or bone marrow reconstitution with IFN-λ-deficient pDC results in reduced expression of homeostatic ISGs in the intestinal epithelium. Notably, intestinal pDC preferentially produce homeostatic IFN-λ, whereas splenic pDC produce Type I IFNs. Comparison of intestinal and splenic pDC reveal tissue-specific changes in gene expression and genomic accessibility, including evidence of responses to transforming growth factor beta (TGF-β) in the intestine. Isolated gut pDC produce more IFN-λ than splenic pDC upon stimulation, and pretreatment of a human pDC cell line with TGF-β results in enhanced transcription of IFN-λ upon stimulation. This study demonstrates that pDC are a substantial source of homeostatic IFN-λ in the intestine and implicates the barrier cytokine TGF-β in regulating IFN types produced by pDC upon stimulation. Reprogramming of recruited pDC by tissue cytokines may have important implications for balancing effective antimicrobial responses with damaging inflammation at barrier tissues.

Animals↗

PubMed2026

Local delivery of interferon restores antigen presentation and sensitizes medulloblastoma to T cell killing.

Medulloblastomas are considered immunologically cold and refractory to immunotherapy. One factor contributing to their low immunogenicity is impaired antigen presentation, which allows tumor cells to evade cytotoxic T cells. Using a syngeneic mouse model of medulloblastoma, we demonstrate that despite low expression of MHC class I on tumor cells, depletion of CD8+ T cells accelerates tumor growth, whereas adoptive transfer of tumor-reactive CD8+ T cells prolongs survival. These antitumor effects rely on T cell-derived interferon gamma (IFNγ), which induces MHC class I on tumor cells and facilitates tumor cell killing by T cells. Importantly, delivering IFNγ directly into tumors via convection-enhanced delivery enhances CD8+ T cell-mediated killing of tumor cells and significantly prolongs survival in tumor-bearing mice. These studies highlight the importance of T cells in controlling brain tumors and the value of IFNγ as an adjuvant for T cell-based immunotherapy.

Animals↗

PubMed2026

The Q653R substitution in the spike protein is associated with attenuation of a GVI-1 infectious bronchitis virus strain.

The GVI-1 genotype of infectious bronchitis virus (IBV) has become increasingly prevalent in Asia. In this study, a highly pathogenic GVI-1 strain (GVI-1-WT) was attenuated by 110 serial passages in embryonated chicken eggs, yielding an attenuated strain (GVI-1-E110). Comparative genomic analysis identified two amino acid substitutions, S523I, Q653R and a nine-amino-acid truncation in the spike (S) protein. To evaluate the contribution of the two point mutations to virulence attenuation, recombinant viruses carrying Q653R and S523I substitutions were generated using a reverse genetics system based on the GVI-1-WT strain as the backbone. Their replication and pathogenicity were assessed in embryonated eggs and specific pathogen-free chickens. The Q653R substitution was associated with reduced viral replication in embryonated chicken eggs and pathogenicity in specific pathogen-free chickens, whereas the S523I mutation alone showed a limited effect but enhanced attenuation when combined with Q653R. However, the attenuation phenotype of the recombinant viruses did not fully recapitulate that of the passaged strain GVI-1-E110, suggesting that additional mutations, including the identified truncation and mutations in replicase-associated genes outside the S protein, may also contribute to virulence attenuation. This study indicates that spike protein mutations are involved in the attenuation of GVI-1 IBV strains, and provides insights into the molecular basis of IBV attenuation during serial passage. Further studies are required to elucidate the underlying mechanisms and to evaluate their potential relevance for vaccine development.

GVI-1 genotype↗

PubMed2026

Puerarin Attenuates Binge Ethanol-Induced Cortical Neurotoxicity in Association with AKT/mTOR Signaling and Autophagy-Related Responses.

Puerarin (Pue), a major isoflavone derived from Pueraria lobata, has demonstrated neuroprotective potential in multiple neurological disorders; however, its effects on ethanol (EtOH)-induced cortical injury and the associated molecular responses remain incompletely understood. In the present study, network pharmacology was combined with in vivo and in vitro experiments to investigate molecular responses associated with the effects of Pue on EtOH-induced neurotoxicity. Public databases were used to predict targets of Pue and alcohol-related brain injury, followed by protein-protein interaction analysis, Gene Ontology annotation, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment. A total of 101 overlapping targets were identified, among which TNF, AKT1, EGFR, TP53, and PPARG emerged as major hub targets, and PI3K-Akt signaling pathway was among the pathways that remained significantly enriched after FDR correction. In a 4-day binge EtOH rat model, Pue attenuated EtOH-associated increases in oxidative stress, neuronal degeneration, and apoptotic markers in cortical tissue. This was accompanied by attenuation of the EtOH-associated reductions in the p-AKT/AKT and p-mTOR/mTOR ratios, as well as an attenuation of EtOH-associated changes in LC3, ATG5, and Beclin-1 expression. In primary cortical neurons, Pue partially attenuated the EtOH-associated loss of neuronal viability and preserved neurite morphology. Bafilomycin A1 (BafA1)-based analysis of LC3-II and p62/SQSTM1 showed an overall BafA1-sensitive increase in LC3-II without a significant treatment-dependent difference in the BafA1 response. Collectively, these findings suggest that Pue attenuates binge EtOH-induced cortical neurotoxicity in association with changes in AKT/mTOR phosphorylation and autophagy-related responses.

AKT/mTOR signaling↗

PubMed2026

Resistance versus concurrent training with three assigned protein targets in middle-aged and older women: a randomized 2 × 3 factorial trial.

BACKGROUND: Evidence is limited regarding whether assigned protein targets modify responses to resistance training (RT) alone or to the same RT program plus cycling (concurrent training [CT]) in middle-aged and older women. This randomized 2 × 3 factorial trial examined bioelectrical impedance analysis (BIA)-derived skeletal muscle mass (SMM; primary outcome), other body composition outcomes, muscular and functional performance, and cycle-derived estimated VO₂max. METHODS: In this randomized 2 × 3 factorial trial, 108 women aged 40-77 years were assigned to 12 weeks of supervised RT or CT (identical RT followed by cycling) and protein targets of 0.8, 1.6, or 2.2 g·kg-1·d-1. Baseline-adjusted ANCOVA tested training × protein interactions and marginal training and protein effects. Complete-case analyses included 83 participants. RESULTS: For SMM, no training-condition × protein-target interaction (p = 0.856), marginal protein-target effect (p = 0.726), or marginal training-condition effect (p = 0.273) was detected. CT had a lower baseline-adjusted week-12 BFP than RT (adjusted difference, -2.04 percentage points; 95% CI, -2.94 to -1.14; p < 0.001). RT had a higher baseline-adjusted week-12 leg-press estimated 1-RM than CT (CT - RT: -6.68 kg; 95% CI, -8.32 to -5.04; p < 0.001), whereas CT had a higher baseline-adjusted week-12 cycle-derived estimated VO₂max (adjusted difference, 4.53 mL·kg-1·min-1; 95% CI, 3.80 to 5.25; p < 0.001). No detectable marginal protein-target effects or training-condition × protein-target interactions were observed for the key secondary outcomes. CONCLUSIONS: No detectable differences in SMM or key secondary outcomes were attributable to assigned protein target. Compared with RT, CT favored estimated aerobic fitness and BFP, whereas RT favored leg-press strength. Because CT included additional cycling and greater exercise exposure, these differences cannot be attributed solely to training modality. Null protein findings do not establish equivalence among doses.

Humans↗

PubMed2026

PSMA1, PSMA5, and PSMB2 serve as prognostic biomarkers and are correlated with tumor-infiltrating leukocytes in HCC.

Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related death. Proteasome (PSM) is the main intracellular proteolytic system in higher eukaryotic cells. It has been reported to be involved in the tumor's onset, metabolism, and survival, and it has been recognized as a therapeutic target for many human cancers. The 20S proteasome subunits, specifically proteasome 20S subunit alpha 1 (PSMA1), proteasome 20S subunit alpha 5 (PSMA5), and proteasome 20S subunit beta 2 (PSMB2), are overexpressed in various malignancies, including HCC. Nevertheless, the exact role of these genes in HCC prognosis remains only partially understood. Moreover, a reliable predictive biomarker for HCC is essential for supporting the implementation of personalized therapies. Therefore, this study employed a comprehensive bioinformatics approach, integrating data from cBioPortal, Human Protein Atlas (HPA), Oncomine, STRING Viruses, Kaplan-Meier plotter, and other established high-throughput databases and tools. The current study thoroughly examined the expression levels, methylation, and genomic alterations of PSM and their correlation with tumor-infiltrating leukocytes. PSMA1, PSMA5, and PSMB2 are overexpressed in various cancers, including HCC, and their expression levels are associated with tumor grade and stage. The abundance of these genes is linked to diminished DNA methylation levels and genome alterations. Moreover, there was a significant association between the expression levels of these genes and poor prognosis and immune cell infiltration. In conclusion, this study proposes PSMA1, PSMA5, and PSMB2 as biomarkers for HCC.

Humans↗

PubMed2026

Integrated metagenomic and metabolomic analysis identifies severity-specific inflammatory and metabolic signatures in post-stroke depression.

Post-stroke depression (PSD) is a common complication that significantly impacts patient prognosis. This study aimed to systematically characterize the associations among gut microbial ecology, metabolic profiles, and inflammatory responses across different severities of PSD. We conducted metagenomic sequencing, non-targeted metabolomics, and serum cytokine analysis (IL-1β, IL-6, IL-10, IL-18, TNF-α, IFN-γ, and CRP) in 91 patients with varying degrees of PSD and non-PSD controls. Bioinformatics analyzes were employed to construct multi-omics association networks and machine learning models. Results indicated that PSD patients exhibited significantly increased gut microbiota alpha-diversity, suggesting dysbiosis. Mild depression was characterized by compensatory neural signaling activation, whereas the moderate depression group exhibited abnormalities in tryptophan/indole metabolism, oxidative stress-related metabolic imbalances, and functional decompensation. Further analyzes suggested that Alistipes, Blautia_A, Evtepia gabavorous, and Lachnospira were associated with inflammatory features, GABA-related metabolic alterations, aromatic amino acid/indole metabolism, and lipid-amino acid metabolism, respectively. Under a more rigorous 10-fold cross-validation framework, the performance of different multi-omics combination models showed heterogeneity; however, some combinations still demonstrated superior discriminatory ability compared to single-omics approaches. This study provides multi-omics clues suggesting associations between different PSD severity levels and features such as increased Alistipes abundance, reduced antioxidant capacity, and altered tryptophan metabolism. It provides candidate biomarker combinations that may be useful for PSD stratification and suggests that the gut microbiome may represent a potential target for future PSD intervention. In summary, PSD may be associated with dynamic alterations along the "gut-brain-inflammation-metabolism" axis. These findings provide integrated evidence for microbial, metabolic, and inflammatory abnormalities across different PSD severity levels, but still require validation in larger samples, longitudinal cohorts, and mechanistic studies.

Humans↗

PubMed2026

Five-year outcomes in a randomised controlled trial of prolonged exposure therapy and supportive counselling for post-traumatic stress disorder in adolescents: a task-shifted intervention.

BACKGROUND: Cognitive-behavioural therapies with a trauma focus are effective in reducing posttraumatic stress disorder and other psychological distress in adolescents. Long-term follow-up data on adolescents treated for PTSD remain scarce, with few studies extending beyond 12 months after treatment completion. OBJECTIVE: To evaluate the maintenance of treatment gains in a comparative study of effectiveness of PE-A and SC up to 60 months post-treatment. METHOD: Sixty-three adolescents diagnosed with PTSD were randomly assigned to either treatment, provided by newly trained and supervised non-specialist health workers. The primary outcome measure was PTSD symptom severity, as independently assessed on the Child PTSD Symptom Scale (CPSS). We report on the 60-month post-treatment follow-up, building on post-treatment, 3-month, 6-month, 12-month and 24-month post-treatment data that have been published previously. RESULTS: Participants in both treatment groups maintained a significant reduction in PTSD symptoms up to 60-months post-treatment (F (7, 343) = 2.86, p < .01). Participants receiving prolonged exposure experienced greater improvement on the CPSS at all follow-up assessment timepoints, except for the 60-month FU (p = .28; g = 0.33). CONCLUSION: Adolescents with PTSD continued to maintain treatment gains up to 60-months post-treatment. These data, along with findings from the original RCT, indicate that a brief treatment protocol (averaging 9 sessions of PE-A or SC) in a LMIC, task-shifted to be delivered by nurses without prior psychotherapy experience, led to lasting improvements in PTSD and comorbid symptoms for up to five years. The sustained benefits and improved functioning over the first few years post-treatment support expanding both treatments, especially PE-A, in community settings.

Humans↗

PubMed2026

Cdk1 and PP2A constitute a molecular switch controlling orderly degradation of atypical E2Fs.

Dynamic oscillations in the phosphorylation and ubiquitination of key proliferative regulators are defining features of the eukaryotic cell cycle. Resetting the cell cycle at the mitosis-to-G1 transition requires activation of the E3 ubiquitin ligase Anaphase-Promoting Complex/Cyclosome (APC/C), which ensures cell cycle irreversibility by targeting dozens of substrates for degradation, safeguarding genome integrity. However, the overall coupling of substrate phosphorylation with target recognition and degradation by the APC/C remains relatively unexplored. As a paradigm for further defining these rules, we focused on E2F7 and E2F8-atypical E2F-family proteins that coordinate cell cycle gene expression by restraining the pro-proliferative transcriptional activity of E2F1. Leveraging complementary cell and cell-free systems, we demonstrate that flexible domains at the amino-termini of E2F7 and E2F8 contain APC/C recognition motifs adjacent to critical Thr residues, whose phosphorylation by Cdk1 is rate-limiting for degradation. The removal of this phosphorylation by PP2A serves as a molecular switch, coupling the degradation of E2F7 and E2F8 to the G1 phase, coinciding with the rise of E2F1. Collectively, these findings highlight a critical role for Cdk1-PP2A signaling in controlling the orderly degradation of APC/C substrates, ensuring precisely timed assembly of the transcriptional infrastructure that coordinates cell cycle commitment and progression.

Protein Phosphatase 2↗

PubMed2026

Mitochondrial uncoupler BAM15 attenuates cryopreservation-induced damage in human sperm by stabilizing mitochondrial homeostasis†.

Human sperm cryopreservation is essential for sperm banking and assisted reproduction, yet freeze-thaw stress promotes oxidative injury that reduces motility and damages the acrosome and nuclear DNA. Here, we tested whether the mitochondrial uncoupler BAM15 improves post-thaw human sperm quality and examined mechanisms linked to mitochondrial homeostasis. Ejaculates were cryopreserved using a standard protocol supplemented with graded concentrations of BAM15. After thawing, total and progressive motility and viability were assessed. Flow cytometry quantified the DNA fragmentation index and the proportion of high DNA stainability cells. Mitochondrial membrane potential, intracellular reactive oxygen species, and lipid peroxidation were measured to evaluate mitochondrial function and oxidative status. Ultrastructural preservation of the acrosome, plasma membrane, midpiece mitochondria, and flagellar axoneme was examined by transmission electron microscopy. Compared with untreated controls, BAM15 increased total and progressive motility and improved viability. BAM15 reduced DNA fragmentation and decreased high DNA stainability, indicating enhanced genomic integrity. Consistently, BAM15 improved mitochondrial membrane potential while suppressing intracellular reactive oxygen species and lipid peroxidation, supporting attenuation of freeze-thaw oxidative damage. Transmission electron microscopy further revealed more continuous acrosomal and plasma membranes, fewer swollen or vacuolated midpiece mitochondria, and improved preservation of axonemal architecture. Collectively, these findings identify BAM15 as a promising cryopreservation supplement that stabilizes mitochondrial homeostasis and improves the functional and structural quality of human sperm after thawing.

Humans↗

PubMed2026

Epigenetic maintenance of male reproductive longevity: SIRT7 as a guardian of male germline genome integrity†.

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Journal Article↗

PubMed2026

Reducing haystacks to needles - ViralClust: A Nextflow pipeline to cluster viral sequences.

BACKGROUND: The rapid accumulation of viral genome sequences presents major challenges for downstream analysis tools, including tools for multiple sequence alignments, phylogeny, and genome/alignment visualization, due to computational constraints and sampling biases caused by outbreak-driven over-representation. Selecting representative genomes through clustering offers a principled alternative to random subsampling, yet choosing appropriate clustering strategies remains non-trivial and context-dependent. RESULTS: Here, we present ViralClust, a modular Nextflow pipeline for bias-aware representative selection from large viral genome datasets. ViralClust integrates five distinct clustering algorithms (CD-HIT-EST, SUMACLUST, VSEARCH, MMSeqs2, and HDBSCAN) within a unified workflow, enabling direct comparison of clustering outcomes and flexible adaptation to diverse biological questions, considering a balanced phylogenetic distribution of the selected sequences. We evaluated ViralClust on six RNA and DNA virus datasets ranging from 632 to 156,586 sequences and spanning genome lengths from 890 to 197,185 nucleotides. Across all datasets, clustering reduced dataset size by ~95 % or more while preserving genetic diversity across species, genera, and families, and effectively mitigating biases introduced by outbreaks, partial genomes, and sequence orientation artifacts. CONCLUSIONS: By supporting whole-genome clustering and scalable representative selection, ViralClust enables efficient and reproducible downstream analyses that would otherwise be computationally infeasible. Rather than offering a prescriptive, guided analysis engine, our framework functions as a flexible comparative collection of complementary strategies, allowing users to empirically evaluate trade-offs and choose the ideal method tailored to their specific analytical endpoints.

Bioinformatics↗