Biology subjects

Xiang, L.

Publications and source records attributed to Xiang, L..

At least 19 recordsLinked to original sources

bioRxiv2026

Torque-optimized body morphing enables rapid surface to underwater diving in whirligig beetles

Known for their rapid water surface locomotion, whirligig beetles (Gyrinidae) are also fast divers. They can transition from the surface to underwater swimming in under 100 ms. Diving requires them to generate sufficient hydrodynamic torque to break the water surface and reorient the body. However, the mechanism by which whirligigs create the necessary pitch-down torque is unknown. Here, we show that their diving is achieved by bending the abdomen. The inertial hydrodynamic pressure on the flexed abdomen generates the torque necessary for surface breaking and body rotation. The torque is maximized at an abdominal angle of 45{degrees}, whereas for effective diving, whirligigs display a preferential abdominal angle of around 28{degrees}, closely aligning with the angle that maximizes the torque-to-drag ratio. This abdominal angle is optimized by balancing torque generation with the drag penalty. Our findings inspire a mechanism for surface-to-underwater transition, offering design principles for multimodal robots capable of locomotion across the air-water interface.

biophysics↗

bioRxiv2026

Single-cell RNA sequencing uncovers cell-type-specific reprogramming of water-channel and cell-wall genes in PFOA uptake by lettuce root tips

Per- and polyfluoroalkyl substances (PFAS) are persistent organic pollutants that accumulate in edible crops, posing threats to food safety and human health. Breeding varieties with reduced PFAS accumulation offers a promising mitigation strategy, yet the underlying cellular mechanisms remain elusive. Here, we integrated short- and long-read single-cell RNA sequencing to generate a high-resolution transcriptomic atlas of lettuce (Lactuca sativa L.) root tips, comparing varieties with contrasting perfluorooctanoic acid (PFOA) accumulation capacities. Our analyses uncovered a synergistic mechanism underlying PFOA uptake: up-regulation of aquaporin genes in epidermal and xylem cells, coupled with down-regulation of cell-wall biosynthesis genes specifically in epidermal and xylem. Furthermore, we identified distinct RNA isoforms-including variants with altered coding potential-that may contribute to PFOA transport and deposition through structural modulation of the encoded proteins. This study represents the first application of single-cell sequencing to elucidate the cellular and molecular basis of crop responses to PFOA, providing new insights into pollutant-crop interactions and informing strategies for sustainable agriculture and food safety.

plant biology↗

bioRxiv2026

AetherCell: A generative engine for virtual cell perturbation and in vivo drug discovery

Virtual cell modeling is currently hindered by a "data-utility paradox": biological information is fragmented between context-rich clinical RNA-seq and perturbation-dense experimental assays, leading to poor predictive generalization in human contexts. Here, we introduce AetherCell, a generative foundation model that unifies these disparate domains into a shared, platform-aligned transcriptomic manifold. By implementing a specificity-driven learning framework, AetherCell successfully recovers low-frequency, mechanism-specific signals often obscured by systematic noise. Across extensive benchmarks, AetherCell demonstrates robust generalization, accurately predicting responses to unseen compounds and genetic perturbations. We show that the model effectively translates signals from simple cell lines to complex 3D organoids, achieving high-fidelity, whole-transcriptome prediction. Building on this foundational manifold, we demonstrate precise drug response prediction across biological scales--including patient-derived organoids and clinical cohorts. We also implement a phenotype-knowledge mixture-of-experts strategy for precision drug repurposing. This approach is validated by the in vivo discovery of teriflunomide for dry eye disease and dabigatran for ulcerative colitis. Together, AetherCell establishes a scalable, human-centric virtual cell framework for translational biology and accelerated drug discovery.

bioinformatics↗

bioRxiv2025

3-Phenylpropionic acid, a microbiota-derived polyphenol metabolite linked to hippuric acid, ameliorates colitis as a colon-enriched PPAR-γ agonist

Polyphenols are promising therapeutics for Crohns disease (CD), yet their bioavailability is largely dependent on the gut microbiome. The bioactive metabolites, metabolic pathways, and anti-inflammatory mechanisms underlying their effects remain poorly defined. We identified hippuric acid (HIPA) as a biomarker of polyphenol-microbiome interaction. HIPA is a meta-organismal metabolite produced through a cross-organ pathway that involves synthesis from gut microbial polyphenol metabolism via 3-phenylpropionic acid (3-PPA), followed by renal clearance. We found that CD is characterised by impaired polyphenol metabolism, resulting in deficient colonic 3-PPA and reduced serum hippuric acid relative to healthy individuals. Furthermore, we demonstrate that 3-PPA is a colon-enriched, mild PPAR-{gamma} agonist that ameliorates colitis in murine model. Systemic bioinformatic profiling of metagenomic data suggested the existence of undiscovered 3-PPA producers. Through targeted microbial incubation with polyphenols, we identified the probiotic Bifidobacterium breve and a lab isolate Escherichia coli FAH as novel 3-PPA producers. Collectively, our findings establish 3-PPA as a diet-dependent, colon-produced, mild PPAR-{gamma} agonist with the potential to minimise adverse effects associated with traditional PPAR-{gamma} agonists. This work establishes a foundation for developing microbiota-targeted, polyphenol-based therapeutic strategies for CD patients.

microbiology↗

bioRxiv2025

Lipid Tail Length Determines Nano-Bio Interactions of Peptide Amphiphile Nanostructures

Understanding the interactions of nanomaterials with biological systems is essential to designing effective nanomedicines. However, most of our understanding originates from studies with solid nanoparticles, and nano-bio interactions of self-assembled nanomaterials have remained largely unexplored. To address this knowledge gap, we develop a series of self-assembling peptide amphiphiles (PAs) with different lipid modifications and investigate their interactions with biological systems. We find that PA nanostructures rapidly disassemble and reassemble with albumin and lipoproteins in blood plasma. While PAs with shorter lipid tails mainly assemble with albumin, increasing lipid length shifts binding to lipoproteins. All PAs show strong tumor accumulation in 4T1 tumor-bearing mice with tumor to liver ratios of [~]3-6. Overall, albumin-binding improves blood circulation and tumor accumulation compared to lipoprotein-binding, but also increases off-target accumulation. This study shows that the biointeractions of self-assembled nanomaterials can be controlled through molecular design, which may lead to the development of effective nanomedicines.

bioengineering↗

bioRxiv2025

Belief updating in uncertain environments are differentially sensitive to reward and punishment learning: Evidence from ERP

Learning from rewards and punishments is crucial for adaptive decision-making, but it is still unclear how individuals integrate prediction errors to update beliefs in uncertain environments, particularly the distinctions between reward and punishment learning. We employed a probabilistic classification task and situated electroencephalography (EEG) signals within a hierarchical Bayesian framework, investigating distinctions between reward and punishment learning. Our findings indicate that participants exhibited superior learning performance in reward context compared to punishment context. Fitting the hierarchical Bayesian model revealed that punishment drives faster Bayesian belief updates, although these did not translate into improved behavioral outcomes. At the neural level, higher-level precision-weighted prediction error (pwPE2) was significantly positively correlated with FRN amplitude in the punishment context but not in the reward context, and the positive effect of pwPE2 on P300 amplitude was stronger in the punishment than the reward condition. These results provide electrophysiological signatures of punish context driving faster belief updates in uncertain environments. Our results provide novel evidence for a dual-process framework in reinforcement learning, underscoring distinct neural mechanisms underlying reward and punishment learning.

neuroscience↗

bioRxiv2025

Precise Extraction of Neural Motifs Reveals Multiscale, Parallel Encoding Schemes in Auditory Cortex

Neural population activity is often stereotyped into recurring activity patterns, i.e., neural motifs, which can be seen as the fundamental building blocks in sensory processing and cognition. In this work we study the codes carried by such neural motifs in primary auditory cortex A1, and analyze how they build on and complement traditional views of single-unit coding. In particular, we study, using two-photon calcium imaging (CI), how activity in A1 differentially represents both sensory stimuli and task and behavioral variables in each of the parallel single neuron and population motif scales. While CI enables the study of neural motifs by capturing the activity of large neural populations, identifying motifs in CI is hampered by the temporal imprecision of current motif-detection algorithms when applied to CI data. We thus developed a new algorithm for motif detection, which enabled us to identify widespread stimulus-encoding motifs as well as a small number of motifs jointly encoding stimulus and choice in Layer 2/3 of A1. These motifs consist of small groups of neurons that are neither clustered nor regularly ordered in space. Interestingly, active neurons within task-encoding motifs exhibit mixed encoding properties inconsistent with the motifs they participate in. Together, these results demonstrate how single unit activity and neural motifs in A1 L2/3 provide different levels of coding granularity containing different information in parallel within the greater neural population. Generally, our results indicate that downstream populations, by selecting which scale of a population drives them, can be selective in the information collected for later cognitive processing.

neuroscience↗

bioRxiv2025

Single-Cell Super-Resolution Quantification of Oxidative DNA Damage via Aptamer-Assisted DNA-PAINT

Accurately quantifying oxidative DNA damage at the single-cell level remains a major challenge due to the limitations of conventional ensemble-based assays, which obscure cell-to-cell variability and lack molecular specificity. To address this, we developed a super-resolution imaging strategy that combines an 8-oxo-dG-specific DNA aptamer with DNA-PAINT, enabling quantitative visualization of 8-oxo-dG lesions with [~]22 nm spatial resolution in individual cells. Our approach reliably detects 8-oxo-dG clusters, distinguishes oxidative damage levels across cells, and exhibits superior specificity and labeling efficiency compared to antibody-based methods. Furthermore, it enables direct evaluation of the repair efficiency of hOGG1 and its catalytic mutants at the single-cell level, overcoming the confounding effects of variable transfection efficiency. This method also serves as a platform for assessing the effects of pharmacological modulators and antioxidants on DNA repair. Looking forward, this strategy can be extended to map other small molecular targets, such as epigenetically modified DNA or RNA bases, with single-cell precision.

biochemistry↗

bioRxiv2025

Glucosylation of Endogenous Haustorium-inducing factors Underpins Kin Avoidance in Parasitic Plants

Parasitic plants rarely attack themselves, suggesting the activity of a kin-avoidance mechanism. In the root parasitic plant Phtheirospermum japonicum, prehaustorium formation is triggered by host-secreted haustorium-inducing factors (HIFs), but it is unresponsive to its own root exudates. Here we report the identification of the spontaneous prehaustorium 1 (spoh1) mutant, which forms prehaustoria without external HIFs. spoh1 harbors a point mutation in the gene encoding UDP-glycosyltransferase GT72B1, an enzyme that glucosylates and thereby inactivates phenolic HIFs. Notably, PjGT72B1 possesses a different substrate specificity from its ortholog of the host Arabidopsis. Introduction of PjGT72B1 in Arabidopsis reduced HIF activity, indicating that HIF glucosylation regulates haustorium induction by hosts. Our findings suggest that parasitic plants have evolved kin-avoidance mechanisms through the glucosylation of endogenous HIFs.

plant biology↗

bioRxiv2025

Senescence-induced reparative fibroblasts enable scarless wound healing in aged murine skin.

It has been reported that elderly individuals exhibit reduced scarring during the wound healing process compared to younger adults. However, the underlying mechanisms responsible for this phenomenon remain poorly understood. Here, we revealed that aged mice exhibited more pronounced regenerative outcomes compared to young mice, characterized by increased hair follicle numbers and collagen fiber features closer to normal skin. Single-cell sequencing identified a reparative fibroblast subpopulation (Prss35+Fib) enriched in the aged group, which promotes regeneration through communication with epithelial cells, macrophages, and T cell subpopulations via PTN and EREG signaling. Spatial transcriptomics validated this communication pattern by elucidating cell proximity and locating the regenerative niche in the upper dermis. Finally, EREG treatment significantly enhanced regenerative outcomes in young mice, while the small wound model of aged mice, lacking the reparative fibroblast and EREG signaling, failed to achieve regeneration. Collectively, our findings advance the understanding of regenerative plasticity in aging and provide new insights for designing scarless therapeutic strategies.

cell biology↗

bioRxiv2025

Super-Resolution Diffusivity Mapping Reveals Spatial Correlations Between Lateral Mobility and Structural Heterogeneities on Cellular Membranes

Cellular membranes orchestrate critical processes such as molecular transport and signal transduction, both regulated by the lateral mobility of lipids and proteins. However, resolving nanoscale diffusional heterogeneities and elucidating their underlying mechanisms remains a formidable challenge due to the membranes intricate architecture and compositional diversity. Here, we present point-cloud single-molecule diffusivity mapping (pc-SMdM), a cutting-edge super-resolution technique that offers a point-cloud data format with enhanced spatial resolution for diffusivity mapping. Using pc-SMdM, we visualize nanoscale diffusion slowdown clusters with [~]50 nm in diameter on plasma membranes. These clusters are predominantly governed by cholesterol content, alongside contributions from membrane protein assemblies and topographical features. Leveraging two-color pc-SMdM, we concurrently imaged multiple lipids and membrane probes, revealing distinct "fingerprint" diffusivity maps shaped by their interactions within lipid bilayers. Our findings position pc-SMdM as a transformative tool for spatially resolving molecular interactions and membrane dynamics in live cells, offering new insights into the underlying mechanisms that govern membrane mobility at the nanoscale.

biophysics↗

bioRxiv2025

CDK12 condensation in nuclear speckles confers sensitivity to cyclin K molecular glue degraders

Transcriptional machinery often operates in the configuration of biomolecular condensates, presenting emerging opportunities to develop therapies targeting transcriptionally addicted malignancies. In this study, we discovered that cyclin-dependent kinase 12 (CDK12), a key regulator of transcription elongation, formed dynamic liquid-like droplets within nuclear speckles, a process enhanced by high CDK12 expression and CDK12 inhibitor treatment. Recognizing this unique property, we rationally designed ZSQ253, a modular cyclin K molecular glue degrader that coupled binding moieties for both CDK12 and DDB1. By promoting phase separation-driven assembly and subsequent proteasomal degradation of the CDK12-cyclin K complex, ZSQ253 interfered with oncogenic transcription and demonstrated potent antitumor capability. Further structure-guided optimization yielded HQY1428, a derivative with a multi-site gluing effect and improved drug activity. Given the frequent genomic co-amplification of CDK12 and ERBB2 across diverse human cancers, we showed that combining HQY1428 with HER2 inhibitors provided synergistic therapeutic benefits. Collectively, our findings establish CDK12 condensation within nuclear speckles as an exploitable vulnerability, and introduce a novel mechanism of action underlying cyclin K molecular glue degraders.

cancer biology↗

bioRxiv2025

Genetic association between posterior parietal cortex and intelligence

The identification of intelligence-associated loci raises questions for functional association of brain regions and for different intelligence concepts of either a general capability or discrete abilities. By generating single-nucleus transcriptomic atlas of mouse posterior parietal cortex (PPC), which is implicated in quantification behavior, we find that human intelligence-associated gene homologs are significantly enriched in certain specific neurons within the PPC. We also find 73% of the human intelligence gene homologs are highly enriched in PPC. In addition to PPC, several regions at different locations, not cortex next to PPC, are also significantly associated with intelligence genes. The separate locations of these cortex regions and their regional-specific expressed intelligence genes raise the possibility for discrete intelligence capabilities. Animal behavior analysis reveals that mutations for two top intelligence-associated genes with specific expression in either PPC or entorhinal cortex (ENT) affect quantification or learning and memory, respectively. Finally, five patients with PPC resection in the left hemisphere also display quantification defects, but not other cognitive abilities. Together, our studies provide the first genetic and functional evidence for the involvement of PPC in intelligence. Our data also support the model of multiple intelligence over a general capability for intelligence.

genetics↗

bioRxiv2025

Automated Discovery of Therapeutic Biomaterial for Renally Impaired Hyperuricemia Patients by Natural Language Processing and Machine Learning

The exponential growth of scientific publications presents opportunities for researchers to identify valuable knowledge, especially in the highly interdisciplinary field --- biomaterials, where exploiting possible connections between unmet clinical needs and materials properties from literatures is crucial. However, with traditional literature reading, it is extremely challenging to marry unmet clinical needs with existing materials reported for different applications or other purposes. Here, to provide a not-renally cleared therapeutics for renally impaired hyperuricemia patients, we designed a multi-tiered framework MatWISE that fuses state-of-the-art natural language processing, semantic relationship mapping, and machine learning to automate the complex process of material discovery from a sea of scientific literatures published until December of 2022, and successfully identified and optimized {delta}-MnO2 into an orally administered, nonabsorbable uric acid (UA) lowering biomaterial. {delta}-MnO2 had superior serum and urine UA-lowering effect in three hyperuricemia mouse models, by comparing with a standard of care drug. {delta}-MnO2 is highly promising to serve as a safe and effective UA-lowering drug for renally impaired hyperuricemia patients. We demonstrated a new research paradigm for biomaterials that combining state-of-the-art machine learning techniques and a handful of experiments to discover a translationally relevant material from the massive existing research, for an unmet clinical need.

biochemistry↗

bioRxiv2025

Development of a novel murine model of in-stent neoatherosclerosis

ObjectiveIn-stent neoatherosclerosis is a phenomenon of percutaneous coronary intervention with stenting. Whilst similar to de novo atherosclerosis, it develops rapidly over 1-5 years rather than over a lifetime. No preclinical small animal models exist that allow full elucidation of neoatherosclerosis biology and future treatments. The aim of this study was to establish and validate a novel murine model of in-stent neoatherosclerosis. Approach and ResultsMurine stainless-steel stents (2.5 x 0.7 mm) were deployed into donor descending aortas of atherosclerosis-prone apolipoprotein (Apo)e-/- mice, then carotid-interposition grafted into Apoe-/- recipients. Mice (n=6-8/group) received chow or a high cholesterol diet (HCD) for 7- or 28-days post-surgery. Multimodal intravascular imaging, simultaneously combining optical coherence tomography (OCT, plaque burden) and fluorescence for indocyanine green (ICG, plaque instability), visualized in-stent neoatherosclerosis across the entire length of the stented site. Histological analyses revealed that stented vessels from mice fed HCD had neointimas with prominent lipid cores and an elevated CD68+ macrophage content, similar to human neoatherosclerosis. Mice fed chow post-stenting had distinctly different neointimas that were smooth muscle cell rich, resembling neointimal hyperplasia. Consistent with this, flow cytometry revealed a higher content of monocytes/macrophages and dendritic cells in stented aortas from mice fed HCD than in non-stented aortas. ConclusionWe have developed and validated the first murine model that replicates the unique characteristics of human in-stent neoatherosclerosis. This project has implications for exploring the mechanisms that promote neoatherosclerosis and testing targeted new therapies. RESEARCH PERSPECTIVEO_ST_ABSWhat Is New?C_ST_ABSO_LIWe have developed and validated a novel murine model of in-stent neoatherosclerosis, presenting a new platform that will facilitate the discovery of novel mechanistic targets of in-stent neoatherosclerosis and preventative therapies. C_LIO_LIThis model develops lesions with a similar morphology to human in-stent neoatherosclerosis and distinct to in-stent neointimal hyperplasia, with higher extracellular lipid and macrophage content and proportionately less smooth muscle cells. C_LIO_LIWe show a first-time visualization of murine in-stent neoatherosclerosis using bimodal intravascular imaging with simultaneous capture of structural information (optical coherence tomography, plaque burden) and the distribution of areas of plaque instability (high-sensitivity fluorescence, indocyanine green) within the plaque. C_LI What new question does this study raise?O_LIHow can the utility of this novel model be maximized as a platform for discovering novel agents that prevent in-stent neoatherosclerosis? C_LI What question should be addressed next?O_LIAre there unique mechanisms of in-stent neoatherosclerosis, distinct to de novo atherosclerosis, that can be specifically targeted to prevent disease and ultimately increase stent performance? C_LI

cell biology↗

bioRxiv2024

Peptide Amphiphiles Hitchhike on Endogenous Biomolecules for Enhanced Cancer Imaging and Therapy

The interactions of nanomaterials with biomolecules in vivo determine their biological fate. Here, we show that self-assembled peptide amphiphile (PA) nanostructures can dynamically interact with endogenous biomolecules and take advantage of naturally occurring processes to target a broad range of solid tumors. In circulation, self-assembled PA nanostructures disassemble and reassemble mainly with lipoproteins, which prolongs blood circulation and dramatically improves tumor accumulation and retention. Mechanistic studies suggested that PAs internalize into cancer cells by assembling with their cell membranes and independently of specific receptors. By exploiting these interactions, a PA developed in this study (namely SA-E) demonstrated specific accumulation in various xenograft, syngeneic, patient-derived xenograft, or transgenic rodent models. In addition, SA-E enabled the effective delivery of highly potent chemotherapy to different syngeneic and xenografted tumors with reduced side effects. With its simple and modular design and universal tumor accumulation mechanism, SA-E represents a promising platform for broad applications in cancer imaging and therapy.

bioengineering↗

bioRxiv2023

Astrocytes gate long-term potentiation in hippocampal interneurons

Long-term potentiation is involved in physiological processes such as learning and memory, motor learning and sensory processing, and pathological conditions such as addiction. In contrast to the extensive studies on the mechanism of long-term potentiation on excitatory glutamatergic synapses onto excitatory neurons (LTPE[->]E), the mechanism of LTP on excitatory glutamatergic synapses onto inhibitory neurons (LTPE[->]I) remains largely unknown. In the central nervous system, astrocytes play an important role in regulating synaptic activity and participate in the process of LTPE[->]E, but their functions in LTPE[->]I remain incompletely defined., We studied the role of astrocytes in regulating LTPE[->]I in the hippocampal CA1 region and their impact on cognitive function using electrophysiological, pharmacological, confocal calcium imaging, chemogenetics and behavior tests. We showed that LTPE[->]I in the stratum oriens of hippocampal CA1 is astrocyte independent. However, in the stratum radiatum, synaptically released endocannabinoids increase astrocyte Ca2+ via type-1 cannabinoid receptors, stimulate D-serine release, and potentiate excitatory synaptic transmission on inhibitory neurons through the activation of (N-methyl-D-aspartate) NMDA receptors. We also revealed that chemogenetic activation of astrocytes is sufficient for inducing NMDA-dependent de novo LTPE[->]I in the stratum radiatum of the hippocampus. Furthermore, we found that disrupting LTPE[->]I by knocking down {gamma}CaMKII in interneurons of the stratum radiatum resulted in dramatic memory impairment. Our findings suggest that astrocytes release D-serine, which activates NMDA receptors to regulate LTPE[->]I, and that cognitive function is intricately linked with the proper functioning of this LTPE[->]I pathway.

neuroscience↗

bioRxiv2023

Co-occurrence of ST412 Klebsiella pneumoniae isolates with hypermucoviscous and no-mucoviscous phenotypes in a short-term hospitalized patient

Hypermucoviscosity(HMV) is a phenotype that is commonly associated with hypervirulence in Klebsiella pneumoniae. The factors that contribute to the emergence of HMV subpopulations remain unclear. In this study, eight K. pneumoniae strains were recovered from an inpatient who were hospitalized for 20 days. Three of the isolates exhibited a non-HMV phenotype, which was concomitant with increased biofilm formation and higher siderophore secretion than the other five HMV isolates. All eight isolates were highly susceptible to serum killing, albeit HMV strains were remarkably more infective than non-HMV counterparts in a mouse model of infection. Whole genome sequencing(WGS) showed that the eight isolates belonged to the K57-ST412 lineage. Average nucleotide identity(ANI) analysis indicated that eight isolates share 99.96% to 99.99% similarity and were confirmed to be the same clone. Through comparative genomics analysis, 12 non-synonymous mutations were found among these isolates, seven of which in the non-HMV variants, including rmpA(R96G) and wbap (S435R), which are assumed to be associated with the non-HMV phenotype. The mutations manB(G440L), dmsB(R193W) and tkt(A643N) occurred in HMV isolates only. RNA-Seq and RT-qPCR revealed transcripts of genes involved in transporter activity, carbohydrate metabolism and energy metabolism, including cysK, paaF, vasD, celC and fruA, to be significantly dysregulated in the non-HMV strain K201060 compared to the HMV strain K201059, suggesting a participation in HMV phenotype development. This study suggests that co-occurrence of HMV and non-HMV phenotypes in the same clonal population may be mediated by mutational mechanisms as well as by certain genes involved in transport and central metabolism. ImportanceK. pneumoniae with a hypermucoviscosity(HMV) phenotype is a community-acquired pathogen that associated with increased invasiveness and pathogenicity, and underlying diseases are the most common comorbid risk factors inducing metastatic complications. HMV was earlier attributed to the overproduction of capsular polysaccharide, and more data point to the possibility of several causes contribute to this bacterial phenotype. Here, we describe a unique event in which the same clonal population showed both HMV and non-HMV characteristics. Studies have demonstrated that this process is influenced by mutational processes and genes related to transport and central metabolism. These finding provide fresh insight into the mechanisms between behind co-occurrence of HMV and non-HMV phenotypes in monoclonal populations as well as potentially being critical in developing strategies to control the further spread of HMV K. pneumoniae.

microbiology↗