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PubMed2026

Uncovering host transcriptional responses to tilapia lake virus (TiLV) through De novo RNA-seq assembly in Nile tilapia, Oreochromis niloticus.

Tilapia lake virus (TiLV) has emerged as an important pathogen that negatively impacts tilapia farming globally. Using RNA sequencing technology, this study investigated the liver transcriptomic profile of apparently healthy and TiLV-infected Oreochromis niloticus from wild. RNA sequence libraries generated 3,356 differentially expressed genes (DEGs), with 1,726 genes that were upregulated. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified 680 different pathways with differential regulation of the metabolic and immune-related pathways indicating that TiLV may interfere in host metabolism and replicate to establish the infection. This study provides transcriptomic insights into the liver responses of naturally TiLV-infected wild O. niloticus and highlights key immune and metabolic pathways associated with viral infection.

Animals↗

PubMed2026

A python based automated computational framework to classify and comparative genomics analysis of the global diversity of chili leaf curl virus (ChiLCV) strains to understand virus host interactions.

Chili leaf curl virus (ChiLCV) is a Begomovirus chillicapsici that is one of the most devastating viruses impacted on the production of chili in the world, especially in South Asia. In the present study, we combined high-throughput computational genomics with experimental analysis of global diversity. A workflow was created using automated Python scripts to download, curate and process ChiLCV genomes from public database. About 410 complete ChiLCV genomes download from public databases. Using a phylogenetic approach, these isolates were subdivided into 34 strains, belonging to 10 major clades, showing significant genetic diversity. Geographic analysis revealed that Pakistan (207 isolates) and India (148 isolates) were the main sources of ChiLCV diversity and the remainder of the isolates were from Oman, Bangladesh, Iran, Saudi Arabia and Sri Lanka. Recombination was observed as a major evolutionary force as more than twenty recombination events were detected. Analysis of cis-regulatory elements showed a complex structure of the viral promoter, including multiple binding sites for transcription factors, hormone-response elements, light-responsive elements, and stress-responsive elements, indicating a high number of interactions between viral regulatory elements and host signaling pathways. Pangenome analysis showed the presence of a highly dynamic open pangenome made up of strain-specific orthologous groups (species-specific orthogroups). Experimental inoculation of chili plants was also carried out to assess the biological effects of infection, along with phytochemical, FTIR, HPLC, and qPCR analyses.

Begomovirus↗

PubMed2026

PTBP1 at the host-virus interface: mechanistic roles in viral RNA translation, replication, and immune modulation.

Viruses require the involvement of host RNA binding proteins for completion of important steps of their life cycle. Polypyrimidine tract binding protein 1 (PTBP1) is an RNA-binding protein found ubiquitously which performs important regulatory functions like alternative splicing, RNA stability, RNA localization, and translation by virtue of its four RRMs and shuttling between nucleus and cytoplasm. There is increasing evidence showing that many viruses make use of such regulatory roles of PTBP1 to facilitate their gene expression and replication. This review describes the existing mechanistic knowledge about the PTBP1 functions during viral infection, paying attention to the role of PTBP1 in viral RNA translation, viral RNA genome replication, and regulation of host antiviral response. Special attention is paid to the regulation by PTBP1 of IRES-dependent translation of enteroviruses and hepatitis C virus, as well as to the PTBP1 contribution to RNA stabilization, long-distance RNA interactions, and genome cyclization of flaviviruses such as dengue virus and Japanese encephalitis virus. Recent data on the PTBP1 function in coronavirus RNA metabolism are discussed as well. Furthermore, the role of PTBP1 in being both proviral and antiviral is reviewed in terms of innate immunity signalling pathways, stress granule biology, and virus-host interaction. Finally, we will explore the possibility of PTBP1 being used as a host-directed antiviral drug target despite the hurdles in doing so considering its multifunctionality as an essential cellular RNA-binding protein.

Polypyrimidine Tract-Binding Protein↗

PubMed2026

Structure-resolved virus-host interactomics by cross-linking mass spectrometry.

Viruses depend on host protein networks to replicate, assemble progeny, and spread between cells and organisms. Defining these virus-host protein interactions is challenging because they are highly dependent on infection stage, cell type, species, and because mechanistic interpretation requires information about structural interfaces and conformational states. Cross-linking mass spectrometry (XL-MS) addresses these challenges by adding a spatial and structural dimension to virus-host interactomics in native systems. In this review, we discuss how XL-MS has advanced from targeted analysis of viral protein complexes to structure-resolved mapping of virion architecture and infected-cell virus-host interactomes. We highlight how XL-MS complements AP-MS, cryo-EM/cryo-ET, quantitative proteomics, genetic perturbation, and structure prediction to connect physical proximity with molecular mechanisms. Finally, we discuss current limitations in sensitivity, chemical coverage, temporal resolution, and model interpretation, and outline how future quantitative and integrative XL-MS workflows may enable systems-level structural virology.

Mass Spectrometry↗

PubMed2026

How elephant host proteins fight-or fail-against EEHV: Insights from a multi-contrast proteomic enrichment study.

Elephant endotheliotropic herpesvirus hemorrhagic disease (EEHV-HD) is a rapidly fatal syndrome of juvenile Asian elephants, but the host-response programs distinguishing progression from survival and the underlying pathophysiology remain poorly defined. The serum proteome of 62 Asian elephants (Elephas maximus) was profiled using a multi-contrast design stratified by age, clinical status, and infection history; protein abundance was analyzed by empirical Bayes linear modeling and Gene Ontology enrichment with semantic similarity reduction. Clinically affected elephants showed enrichment of inflammatory and stress-associated processes-including cytokine signaling and chromatin remodeling-with suppression of type I interferon signaling and homeostatic functions, whereas asymptomatic exposed elephants showed enrichment of metabolic pathways, including fatty acid and pyruvate metabolism, vesicle-mediated transport, and protein quality control. Disease-versus-exposure comparisons distinguished a progression program (inflammatory escalation with loss of proteostasis and cell adhesion) from a resilience program (preserved metabolic and cellular homeostasis); juvenile susceptibility was further associated with impaired lipid and calcium regulation and disrupted intracellular transport. Collectively, these patterns support a pathology-centered model in which fatal EEHV-HD reflects endothelial injury coupled with maladaptive inflammation and metabolic failure. Protein-level interpretation identified candidate drivers of inflammatory amplification, endothelial barrier disruption, coagulation imbalance, and resilience-including JAK1, IL1RL2, IFI44, KCNJ15, MSN, HECW2, ITPR3, MFN2, AKT1, BMPER, and DROSHA-providing a mechanistic bridge between serum proteomic changes and the vascular lesions, thrombocytopenia, DIC-like coagulopathy, edema, and hemorrhage of EEHV-HD. These findings nominate candidate proteomic signatures for future diagnostic and risk-stratification studies; longitudinal individual-level validation is required before clinical application. Because diagnostic screening identified all PCR-positive sick cases as EEHV1A and pooled group-level serum profiles were analyzed, these signatures should be interpreted as exploratory host-response programs specifically reflecting acute EEHV1A disease requiring individual-level validation.

Animals↗

PubMed2026

Human endogenous retroviruses leading to autoimmune diseases.

Human endogenous retroviruses (HERVs) comprise approximately 8% of the human genome and were long regarded as inert remnants of ancestral retroviral infections. Increasing evidence indicates that HERVs are active genomic elements capable of influencing transcriptional programs, modulating immune responses, and contributing to disease pathogenesis. Under physiological conditions, HERV expression is tightly controlled by epigenetic mechanisms; however, infections, chronic inflammation, aging, and diverse environmental stimuli can promote HERV reactivation. HERV-derived RNAs and proteins engage innate immune sensors and trigger antiviral-like responses through mechanisms of viral mimicry, leading to activation of type I interferon and other inflammatory pathways. HERV dysregulation has been associated with disease-relevant immune pathways. This review summarizes recent advances linking HERVs to autoimmune disease pathogenesis and discusses their potential translational relevance as biomarkers and therapeutic targets.

Humans↗

PubMed2026

Host Proteome Remodeling During Group A Streptococcus Skin Infection.

Group A Streptococcus (Streptococcus pyogenes, GAS) is a bacterial pathogen that commonly causes local infections in humans and can lead to invasive diseases. GAS infections trigger complex host immune and tissue responses, yet how these processes are coordinated over time and across different tissues remains poorly understood. To explore the spectrum of GAS infection, we examined responses in a skin infection model at multiple proteome levels, characterizing local and distant tissues with variable infection responses. We map changes in canonical innate and adaptive immune signaling while uncovering new mechanisms in the context of skin infection. We uncover the robust and time-dependent expression of one family of proteins, chitinase-like proteins, that coincides with immune cell infiltration of local tissues. Because immunomodulatory networks are tightly regulated through post-translational modifications, we integrated global proteomic data with cytokine signaling and key phosphoproteome changes. This analysis revealed correlations between mTOR and kinase signaling pathways that diverge at local and systemic tissues. Our systems-based approach provides a rigorous evaluation of a GAS skin infection, characterizing host proteome remodeling across experimental groups and individual mice.

Animals↗

PubMed2026

S-layer-phage interaction in Clostridioides difficile.

Successful infection by a bacteriophage requires the injection of the phage genome into the cytoplasm of the host bacterium. To achieve this, an infecting phage must traverse the layers of the host cell envelope, including the membrane(s) and the cell wall. This process is further complicated in bacterial species that produce a proteinaceous S-layer on the outermost surface of the cell. Surprisingly little is known about the mechanistic basis of these early stages in the phage lifecycle, and even less is known about infection of S-layer producing bacteria. Recent advances in structural biology, particularly in cryoEM, have dramatically improved our understanding of the structures of both bacterial S-layers and phage virions separately, but we still lack a molecular view combining both phage and S-layer in the process of infection. Here, we review our current understanding of phage-S-layer interactions, using the human pathogen Clostridioides difficile as an example host.

Clostridioides difficile↗

PubMed2026

TRIM21 induces selective autophagy of viruses and bacteria.

TRIM21 is an exceptionally versatile ubiquitin ligase that can be directed by antibodies to target oligomeric protein scaffolds, viral capsids, and proteopathic aggregates for intracellular degradation. How the cell degrades these typically resistant substrates remains poorly understood. To address this, we used TRIM21 viral restriction to create a genome-wide phenotypic screen for antibody-dependent capsid degradation. We identify an antimicrobial selective macroautophagy pathway in mammalian cells, which we term "antibody-directed xenophagy" (ADX). We show that this mechanism restricts structurally diverse pathogens, including adenovirus and Salmonella. Using quantitative microscopy, we demonstrate that TRIM21 rapidly intercepts antibody-pathogen complexes, leading to ubiquitin ligase activation. Following this, selective autophagy adaptors are recruited, and viral cargoes are delivered to lysosomes. This process reduces Salmonella pathology and bacterial tissue invasion in mice. We propose that TRIM21 evolved through competition with pathogens to induce autophagy of diverse and complex substrates, potentially explaining its versatility for targeted protein degradation.

TRIM21 Protein↗

PubMed2026

Glycaemic burden disrupts innate immunity in TB by modulating CD206 expression and macrophage antimicrobial responses.

Tuberculosis (TB) and diabetes mellitus (DM) represent a growing dual global health burden, with chronic hyperglycaemia recognized as a major modifier of host immunity against Mycobacterium tuberculosis (Mtb). Macrophages, central to pathogen recognition, phagocytosis, antigen presentation, and intracellular killing, may be particularly vulnerable to diabetic metabolic dysregulation. This study evaluated phenotypic and functional macrophage alterations in individuals with pulmonary TB, type 2 DM, TB-DM comorbidity, and healthy controls. Surface receptor expression was analysed by multicolour flow cytometry, while phagocytosis and intracellular bacterial clearance were assessed using FITC-labelled Mtb assays and colony-forming unit enumeration. Hyperglycaemia was associated with reduced CD11b, MARCO, and TLR2 expression alongside upregulation of the mannose receptor CD206, which correlated positively with HbA1c levels, indicating a shift toward a permissive M2-like phenotype. Phagocytic uptake of Mtb was significantly impaired and inversely correlated with HbA1c. Antigen-presenting capacity was selectively compromised, with reduced CD80 and CD86 expression in DM and TB-DM groups, while HLA-DR remained unchanged. Intracellular Mtb killing was markedly diminished in diabetic macrophages. These findings demonstrate that chronic hyperglycaemia profoundly disrupts macrophage innate immunity, contributing to increased TB susceptibility and poor infection control in diabetic populations.

Humans↗

PubMed2026

Conserved host-exclusive oligonucleotide motifs enriched in pathogenic genes of human oncogenic viruses.

Comparative viral genomics can reveal sequence-level constraints influencing virus-host interactions. Relative minimal absent words (rMAWs) are short oligonucleotide motifs present in viral genomes but completely absent from the host, potentially reflecting selective pressures related to host adaptation and immune evasion. Using the EAGLE algorithm and the GRCh38 human reference genome, we systematically screened for prevalent rMAWs (prMAWs) across six major human oncogenic viruses: Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), human T-cell leukemia virus type 1 (HTLV-1), and human herpesvirus 8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV). highly conserved 11- and 12-bp prMAWs were identified in EBV, HBV, HTLV-1, and HHV-8/KSHV, with sequence prevalences ranging from 91.5% to 97.9%. Conversely, no short prMAWs were detected in HCV or HPV, likely reflecting differences in genome architecture, mutation rates, and long-term host adaptation to the human host. Importantly, the identified host-exclusive motifs exhibited non-random genomic distribution and were preferentially embedded within viral genes central to replication, persistence, immune modulation, and oncogenesis, including EBNA-1 (EBV), HBx (HBV), Tax-associated regions (HTLV-1), and lytic replication genes of HHV-8/KSHV. Notably, all detected prMAWs were enriched in GC nucleotides and exhibited marked CpG over-representation, suggesting sequence constraints associated with epigenetic regulation and viral persistence. Collectively, these highly conserved, host-exclusive signatures offer promising, candidates for sequence-directed approaches in the diagnosis, monitoring, and investigation of virus-associated cancers.

Humans↗

PubMed2026

Potato purple top phytoplasma infection induces autophagy-associated lipid dynamics that support pathogen proliferation.

Phytoplasmas are unculturable, phloem-restricted bacterial pathogens responsible for devastating diseases in crops and ornamentals worldwide. Their mechanism for nutrient acquisition from host plants remains largely unknown. This study demonstrated that infection with potato purple top phytoplasma induced extensive remodeling of lipid metabolism in tomato plants, closely linked to autophagy activation. Western blot and confocal analyses revealed increased ATG8 lipidation and autophagosome formation at endoplasmic reticulum stress sites, alongside the redistribution of lipid droplets toward phytoplasma cells. Lipidomic profiling showed a decline in chloroplast galactolipids and phospholipids with a concomitant rise in triacylglycerol, indicating accelerated membrane turnover and neutral lipid sequestration. Transmission electron microscopy further revealed frequent spatial proximity between lipid droplets and phytoplasmas. Inhibition of autophagy with 3-methyladenine blocked lipid droplet breakdown, disrupted endoplasmic reticulum organization, and reduced phytoplasma titers, suggesting that host autophagy contributes to phytoplasma proliferation. In addition, genome analysis identified a conserved phytoplasma-encoded alpha/beta hydrolase (potato purple top-lipase), predicted to be related to monoacylglycerol lipases. In vivo assays in yeast and Nicotiana benthamiana confirmed that potato purple top-lipase reduced neutral lipids, mainly triacylglycerol, and that catalytic triad mutations abolished activity. Because potato purple top-lipase lacks a predicted secretory signal peptide, it likely functions intracellularly within phytoplasma cells and may participate in the metabolism of lipid intermediates. These findings support a model in which phytoplasma infection is associated with host autophagy-associated lipid droplet mobilization and a phytoplasma lipase that may contribute to host-derived lipid resources, providing insight into potential nutrient acquisition strategies of phloem-restricted pathogens.

Autophagy↗

PubMed2026

A Novel Approach to Engineering Tomato Spotted Wilt Virus Infectious Clones by Disarming Key Nodes in Antiviral Defenses.

Tomato spotted wilt virus (TSWV) is an economically devastating pathogen that rapidly overcomes genetic resistance in major crops. Reverse genetic systems are crucial for investigating plant-virus interactions and resistance-breaking mechanisms, and developing these tools for segmented ambisense RNA viruses remains a crucial challenge. Current TSWV clones rely on extensively modified Asian isolates requiring co-delivery of multiple replication helpers and viral silencing suppressors. Streamlining these systems for regionally significant strains with minimal genetic alterations is essential. Here, we developed the first infectious clone of a U.S. TSWV isolate (PA01). Three binary plasmids contain cDNAs for the antigenomic L and S segments, as well as the genomic M segment, with enhanced GFP replacing NSs on the S segment. Co-delivery of the cucumovirus 2b alone or in combination with tombusvirus P19 or begomovirus AL2 achieved a high proportion of systemically infected Nicotiana benthamiana and Capsicum annuum plants. In N. tabacum, co-delivering the Caenorhabditis elegans cell death suppressor CED-9 or using NahG transgenic plants produced 30 to 33% systemically infected plants. Co-delivery of 2b boosted infection levels in NahG plants to 62%. These data indicate that in addition to the antiviral RNA-silencing machinery, additional host defense pathways influence TSWV rescue and systemic infection from cDNA. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Tospovirus↗

PubMed2026

Time-resolved mapping in calves reveals bovine herpesvirus 1 shift from mucosal replication to trigeminal ganglion neuroinvasion with promyelocytic leukemia protein-centered host-virus antagonism.

Although bovine herpesvirus 1 (BoHV-1) causes massive losses of cattle, the transition from mucosal replication to neuroinvasion remains poorly understood. Using a controlled calf model, we integrated quantitative virology and transcriptomics to map its pathogenesis and define the role of promyelocytic leukemia protein (PML). Calves inoculated intranasally and ocularly (1.4 × 106 plaque-forming units/head) were sampled daily (1-14 days post-infection, dpi) for glycoprotein B (gB) qPCR. Tissues were analyzed at 4 and 14 dpi to measure viral DNA via gB-specific qPCR, and for mRNA-seq of trigeminal ganglia (TG). Shedding peaked at 3-6 dpi, being highest in nasal samples, lower in ocular samples, and substantially lower in rectal samples, and declined by 10-14 dpi. At 4 dpi, among the tissues sampled, the tonsils exhibited the highest viral burden. TG exhibited low viral levels at 4 dpi, although they remained detectable at 14 dpi, indicating neuroinvasion. The TG program shifted from early proteostasis priming (4 dpi) to immune/extracellular matrix activation with synaptic repression (14 dpi). In MDBK/Vero cells, IFN-α resulted in higher bovine PML (bPML) levels and enlarged PML nuclear bodies (PML-NBs), reducing very early viral DNA levels, whereas BoHV-1 disrupted PML-NB integrity. The different bPML isoforms exerted different effects on viral infection. STRING analysis revealed a conserved PML-SUMO1-UBE2I-DAXX-SP100 core. These findings delineate the mucosal-to-neuronal trajectory, establish PML as both an effector and viral target in complementary in vitro systems, and identify SUMO/ubiquitin-linked proteostasis as a tractable target for antiviral intervention.IMPORTANCEAlthough bovine herpesvirus 1 (BoHV-1) remains a major challenge to cattle health, the early transition from mucosal replication to trigeminal neuroinvasion has not been clearly mapped in natural-host calves. By integrating daily shedding kinetics, tissue viral DNA profiling, and time-resolved trigeminal ganglion transcriptomics, we delineate when and how BoHV-1 reaches the sensory neurons. Promyelocytic leukemia protein (PML) is identified as a key intrinsic antiviral factor that is upregulated by IFN-α and restricts very early viral genome accumulation, while viral BoHV-1-encoded infected cell protein 0 actively dismantles PML nuclear bodies. The discovery of opposing isoform-specific PML functions and a conserved PML-SUMO proteostasis hub provides mechanistic insight into BoHV-1 immune evasion. These findings refine our understanding of the mucosal-to-neuronal trajectory of infection and highlight proteostasis-linked antiviral pathways as promising targets for intervention.

Animals↗

PubMed2026

TALEs, TALENs, and TALE Base Editors: From Plant Pathology to Biotechnology.

TALEs (transcription activator-like effectors) are an excellent example of how studying pathogen-host interactions can lead to significant biotechnology inventions. TALEs are bacterial effectors that are translocated into plant cells via a bacterial type III secretion system. Once inside the host cell, they are imported into the nucleus to bind specific promoters and induce expression of target genes, thereby supporting the bacterial infection. TALEs are found throughout many, but not all, Xanthomonas pathovars, which can be severe pathogens of different crops. The key feature of TALEs is their modular DNA-binding domain, which allows a simple evolutionary adaptation to novel DNA sequences as well as simple cloning of designer TALEs with desired DNA-binding specificity. Accordingly, TALE nucleases started the genome-editing revolution, and TALE base editors are the latest tools to efficiently edit chloroplast and mitochondrial genomes. We review recent advances in Xanthomonas genomics, synthesize current knowledge about naturally occurring TALEs, and highlight current roles of TALEs in genome editing and synthetic biology.

Xanthomonas↗

PubMed2026

Shining Light on Late Blight.

In this retrospective on my journey in science, I shine light on the ins and outs of the late blight pathogen Phytophthora infestans. While studying plant pathology, I became fascinated by the molecular mechanisms that govern the development of cells and organisms and ended up unraveling intimate plant-microbe interactions. I have been fortunate to work in an inspiring environment and with committed coworkers. I am proud of what we achieved as a team. By digging into the biology of Phytophthora and exploring genomes and pathogenicity mechanisms, we uncovered a treasure trove of novelties and peculiarities that offer ample opportunities for designing pathogen-informed control strategies.

Plant Diseases↗

PubMed2026

Tree Killer, Qu'est-ce Que C'est? Insights From Forest Pathogen Genomes.

Forests are central to planetary health but are increasingly challenged by emerging diseases driven by climate change, global trade, and anthropogenic disturbance. Despite the apparent resilience of long-lived, genetically diverse tree hosts, forest ecosystems have repeatedly experienced landscape-level pathogen-driven transformations. Advances in genomics, transcriptomics, and functional biology have transformed our understanding of how fungal and oomycete pathogens interact with their hosts across a continuum of lifestyles, from saprotrophy and necrotrophy to biotrophy. Here, we synthesize insights from comparative and population genomics and functional studies across diverse forest pathosystems to examine the traits that characterize successful tree pathogens. We highlight how lifestyle plasticity, adaptations to woody tissues, vector-mediated transmission, and biotrophic stealth enable pathogens to colonize perennial hosts and persist over long temporal scales. We further examine how genome plasticity, hybridization, and horizontal gene transfer generate adaptive potential that often outpaces host evolutionary responses under current environmental change. Finally, we discuss emerging genomic tools, including biosurveillance, machine learning-based classification, and genome editing, that are beginning to link genotype to phenotype and inform assessments of disease risk. By integrating genomic, ecological, and evolutionary perspectives, this review outlines general principles governing forest pathogen success and identifies priorities for future research aimed at improving understanding, early detection, and management of forest diseases in a changing world.

Trees↗

PubMed2026

Parallel single-cell host immune profiling and pathogen genomic characterization in Klebsiella-associated sepsis: a pilot study.

OBJECTIVES: Sepsis is a life-threatening syndrome characterized by profound immune dysregulation and substantial biological heterogeneity. Here, we conducted a pilot study to explore host immune remodeling in Klebsiella-associated sepsis by combining single-cell RNA sequencing of peripheral blood mononuclear cells with whole-genome sequencing of the corresponding bloodstream isolates. METHODS: In this prospective observational pilot study, we analyzed peripheral blood mononuclear cells (PBMCs) from two patients with Klebsiella-associated sepsis and two healthy controls (HC) using single-cell RNA sequencing. PBMC composition, differential transcriptional responses, and pathway analysis were assessed across immune subsets. The corresponding bloodstream isolates were characterized by phenotypic antimicrobial susceptibility testing and whole-genome sequencing. RESULTS: Compared to HC, septic patients showed expansion of the myeloid compartment and contraction of the NK/T compartment. High-resolution analysis suggested shifts within lymphoid populations. At the transcriptional level, sepsis was associated with compartment-specific enrichment of interferon-related and host-defence pathways, as well as oxidative phosphorylation, ATP synthesis, and mitochondrial electron transport signatures across multiple PBMC subsets. Classical monocytes exhibited a coordinated decrease in MHC class II-related transcripts. The sepsis-associated isolates were identified as Klebsiella pneumoniae and Klebsiella variicola and were notable for overall antimicrobial susceptibility, limited resistomes, and absence of canonical hypervirulence determinants. CONCLUSION: Our data provide a preliminary description of immune remodeling during Klebsiella-associated sepsis and suggest that severe clinical disease may be associated with isolates lacking classical multidrug-resistance or hypervirulence features. These findings should be interpreted as preliminary and hypothesis-generating and require validation in larger cohorts with detailed clinical severity assessment.

Female↗