Biology subjects

Lyu, L.

Publications and source records attributed to Lyu, L..

18 recordsLinked to original sources

bioRxiv2026

AutoScreen: AI Co-Scientist System for Target Discovery in Functional Genomics

Target discovery in functional genomics remains largely manual and time-consuming, lacking systematic tools for efficient and reproducible gene-level hypothesis generation. We introduce AutoScreen, an AI co-scientist system supporting target discovery through both Pre-screen Design, which constructs perturbation libraries de novo from free-text research descriptions, and Post-screen Analysis, which re-ranks experimental screen hits by integrating statistical scores with biological context. AutoScreen leverages the complementary strengths of multiple specialist agents that perform deep research into multi-modal evidence, information restructuring, parallel searches across >26 biomedical databases, evidence synthesis, and target review to provide transparent, explainable gene prioritization with pipeline provenance. Across 320 genome-scale CRISPR screens as expert-curated benchmarks, AutoScreen achieved a ~19% increase in validated-hit recovery among its top 100 predictions, relative to the strongest agent baseline, and required a 1.2-fold smaller library to recover the same number of hits at the top-500 reference point. AutoScreen reached mean average precision more than two orders-of-magnitude above random baseline. Further, we validated AutoScreen in cancer immune-evasion case studies focusing on natural killer (NK) and T-cell therapeutics. AutoScreen recovered NK-resistance genes that were initially lower-ranked in a leukemia screen, moving MUC1, PDPN, and LRRC15 from raw ranks of 118, 81, 1384 to 5, 44, 659, respectively. In follow-up tumor killing assay with primary human NK cells, individual perturbation validated all three hits successfully. Next, in prospective benchmarking across two cytotoxic T-cell-killing screens, AutoScreen recovered 77.1% of ground-truth hits called by the consensus of two gold-standard analysis pipelines (FDR<0.1), achieving 8% improvement over the strongest general-purpose LLM agent baseline. Finally, we re-analyzed >500 public datasets to construct the AutoScreen Resource Hub, a growing knowledge base of pre-computed, annotated reports for CRISPR screens, RNA-seq differential expression, and gene-level UK Biobank genome-wide association studies. This agentic AI approach enables real-time genomics benchmark construction that are continuously updated, expanded, for evaluating frontier AI co-scientists. Overall, AutoScreen enables AI-powered target discovery to be more auditable, scalable, extensible, and reproducible.

bioengineering↗

bioRxiv2026

CellAwareGNN: Single-Cell Enhanced Knowledge Graph Foundation Model for Drug Indication Prediction

Graph foundation models have emerged as powerful tools for drug repurposing by enabling the prediction of novel drug-disease indications from large biomedical knowledge graphs. A representative example is TxGNN, which was previously developed and trained on PrimeKG, a comprehensive biomedical knowledge graph covering over 17,000 diseases. While TxGNN demonstrates strong performance, existing biomedical knowledge graphs largely lack fine-grained, cell-type-specific expression context. This limits their ability to capture disease mechanisms driven by dysregulated cellular programs, such as immune cell-specific pathways in autoimmune diseases. Moreover, prior evaluations typically test only randomly selected subsets of diseases, leaving many diseases unexamined and limiting conclusions about model performance across the full disease spectrum. To address these limitations, we first update PrimeKG to PrimeKG-U by incorporating expanded and curated biomedical knowledge and then develop TxGNN-U as a stronger graph-based baseline. Building on this foundation, we introduce CellAwareGNN, a graph foundation model that integrates single-cell genomics into PrimeKG-U. We construct a single-cell-enhanced knowledge graph, scPrimeKG, by incorporating cell-type-specific gene expression signatures from the OneK1K dataset, expanding PrimeKG from approximately 8.1 million edges and 129k nodes to over 14 million edges and 147k nodes. CellAwareGNN is pre-trained on all relation types in scPrimeKG and evaluated on drug indication prediction with explicit coverage of all diseases in the knowledge graph. CellAwareGNN consistently outperforms TxGNN and TxGNN-U. For drug indication prediction, CellAwareGNN achieves an AUPRC of 0.826, representing a 1.2% improvement over TxGNN-U (0.816) and a 3.4% improvement over TxGNN (0.799). Notably, for autoimmune diseases, CellAwareGNN attains an AUPRC of 0.864, improving by 2.0% over TxGNN-U (0.847) and 6.0% over TxGNN (0.815). Importantly, CellAwareGNN prioritizes promising repurposing candidates, including Ocrelizumab for Pemphigus via CD20-expressing B cells, Methotrexate for Pemphigus through DHFR and ATIC activity in T and B cells, and Rosiglitazone for Rheumatoid Arthritis through PPAR-{gamma} activation. These results demonstrate the value of incorporating cell-type-specific expression context to improve both predictive performance and biological interpretability in graph-based drug repurposing. CCS ConceptsO_LIApplied computing [->] Health informatics; Bioinformatics; C_LIO_LIComputing methodologies [->] Knowledge representation and reasoning; Neural networks. C_LI ACM Reference FormatXinmeng Zhang, Eugene Jeong, Chao Yan, Yubo Feng, Linshuoshuo Lyu, Xingyi Guo, and You Chen. 2026. CellAwareGNN: Single-Cell Enhanced Knowledge Graph Foundation Model for Drug Indication Prediction. In Proceedings of the 32nd ACM SIGKDD Conference on Knowledge Discovery and Data Mining V.2 (KDD 2026), August 9-13, 2026, Jeju Island, Republic of Korea. ACM, New York, NY, USA, 12 pages. https://doi.org/10.1145/3770855.3819012

bioinformatics↗

bioRxiv2026

N6-methyldeoxyadenosine is a transgenerational epigenetic mark protecting DNA from deletion

DNA N6-adenine methylation (6mA) is emerging as an important DNA modification present in all eukaryotic kingdoms, where its roles mostly involve transcriptional regulation and chromatin modification. Here, we demonstrate a distinct role for 6mA in Paramecium tetraurelia. We find that it is a trans-generational epigenetic mark which distinguishes host DNA from invasive elements, protecting the former. During development, Paramecium deletes around 25% of its germline genome, removing TEs, repetitive sequences and transposon-derived elements, to form a functional somatic genome. We show that 6mA is present in the Paramecium germline nucleus, where it is preferentially located on host DNA and excluded from TEs. Ectopic addition of 6mA to germline DNA causes failure to excise TE-derived sequences, leading to lethality. 6mA presence on a synthetic TE-derived element is sufficient to block its excision during development. These effects are inherited via sexual reproduction, demonstrating their trans-generational capacity.

cell biology↗

bioRxiv2025

Molecular mechanism of the key dormancy regulator DosR-dependent transcription activation in Mycobacterium tuberculosis

Mycobacterium tuberculosis (Mtb) is the etiological agent responsible for the worldwide disease Tuberculosis. DosR is recognized as the key dormancy regulator of Mtb due to its global transcriptional regulation in intracellular adaptation and long-term persistence prevailing in latent infection. However, the molecular mechanism regarding DosR-dependent transcription activation remains inadequately defined. Here, we successfully determined the cryo-EM structure of an intact DosR-dependent transcriptional activation complex (DosR-TAC), comprising Mtb RNA polymerase (RNAP), DosR, and the hypoxic promoter DNA. In DosR-TAC, two DosR monomers symmetrically dimerize through their N-terminal receiver domains (DosR_RECs) and the distinct 10 helices of the C-terminal DNA-binding domains (DosR_DBDs). Unlike its inhibitory configuration, the DosR dimer undergoes significant conformational changes within the original linker, isomerizing DosR_REC into a canonical ({beta})5 fold. This extended linker affords the DosR_DBDs and DosRI_REC to contact promoter DNA, while concurrently interacting with the conserved domains of RNAP ({sigma}AR4, CTD, and NTD). Additionally, RT-qPCR and growth curve assays of the wild-type and DosR mutant strains, also unravel the physiological importance of this divergent linker. These findings, together with prior hypotheses regarding DosR, support an allosteric activation-recruitment model for DosR. Altogether, these results highlight the molecular mechanism of DosR-dependent transcription activation critical for dormancy survival of Mtb, and offer potential targets for developing anti-dormancy strategies against persistent tuberculosis.

microbiology↗

bioRxiv2025

CSCN: Inference of Cell-Specific Causal Networks Using Single-Cell RNA-Seq Data

Understanding gene regulation is fundamental to deciphering the coordinated activity of genes within cells. Although single-cell RNA sequencing (scRNA-seq) enables gene expression profiling at cellular resolution, most gene network inference methods operate at the tissue or population level, thereby overlooking regulatory heterogeneity across individual cells. Recent approaches, such as Cell-Specific Network (CSN) and its extension c-CSN, attempt to construct gene networks at single-cell resolution, providing a more detailed view of the regulatory logic underlying individual cellular states. However, these methods remain limited by high false positive rates due to indirect associations and lack of directionality or causal interpretability. To address these issues, we propose the Cell-Specific Causal Network (CSCN) framework, which infers directed, cell-specific gene regulatory relationships by explicitly modeling causality. CSCN combines causal discovery techniques with efficient computation using kd-trees and bitmap indexing to perform conditional independence testing, yielding sparse and interpretable causal graphs for each cell that effectively suppress indirect and spurious associations. We demonstrate through simulations that CSCN significantly reduces false positives compared to existing methods. Furthermore, we evaluate the quality of the inferred causal networks via clustering on the Causal Katz Matrix (CKM), and CSCN outperforms CSN and c-CSN in distinguishing cellular states.

bioinformatics↗

bioRxiv2025

Suppression of interferon signaling via small molecule modulation of TFAM

The mitochondrial transcription factor A (TFAM) is essential for mitochondrial genome maintenance. It binds to mitochondrial DNA (mtDNA) and determines the abundance, packaging and stability of the mitochondrial genome. Because its function is tightly associated with mtDNA, TFAM has a protective role in mitochondrial diseases and supportive studies demonstrate reversal of disease phenotypes by TFAM overexpression. In addition, TFAM deficiency has been shown to cause release of mtDNA into the cytosol and activation of the cGAS/STING innate immune response pathway. As such, TFAM presents as a unique target for therapeutic intervention, but limited efforts for activators have been reported. Herein we disclose novel TFAM small molecule modulators with sub-micromolar activity. Our results demonstrate that these compounds result in increase of TFAM protein levels and mtDNA copy number. This results in inhibition of a mtDNA stress-mediated inflammatory response by preventing mtDNA escape into the cytosol. Furthermore, we see beneficial effects in cellular disease models in which boosting TFAM activity has been advanced as a disease modifying strategy including improved energetics in MELAS cybrid cells and a decrease of fibrotic markers in Systemic Sclerosis (SSc) fibroblasts. These results highlight the therapeutic potential of using small molecule TFAM activators in indications characterized by mitochondrial dysfunction.

cell biology↗

bioRxiv2025

Programmable macromolecule delivery via engineered trogocytosis

Trogocytosis, the transfer of plasma membrane fragments during cell-cell contact, offers potential for macromolecular delivery but is limited by uncertain fate of trogocytosed molecules, constraints to membrane cargo, and unclear generalizability. Here, we demonstrate that donor cells engineered with designed receptors specific to intrinsic ligands can transfer proteins to recipient cells through direct contact. We identified key principles for enhancing contact-mediated transfer and subsequent functionalization of transferred macromolecules, including receptor design, pH-responsive membrane fusion, inducible cargo localization, release, and subcellular translocation. Exploiting these findings, we developed TRANSFER, a versatile delivery system that integrates logic gate-based control to sense multiple ligand inputs and deliver diverse functional cargos for genome editing and targeted cell ablation across cell types. The study establishes trogocytosis as a novel, programmable framework for cell-based macromolecular delivery.

bioengineering↗

bioRxiv2024

Comprehensive analysis of macrophages infected with avirulent and virulent Mycobacterium tuberculosis uncovers distinct immune mechanisms and anti-TB effect of treated exosomes

Tuberculosis (TB) is now the worlds second deadliest infectious killer after COVID-19. Human-macrophages and their secreted exosomes play important roles in combating invading Mtb. However, the panoramic analysis of the underlying immune mechanism for the infected macrophages, package or secretion mechanism, and anti-TB effect of Mtb treated exosomes remain poorly understood. Here we conducted comprehensive analyses of the macrophages infected with avirulent and virulent Mtb (H37Ra & H37Rv) and their secreted exosomes, collected cells and corresponding exosomes for omics and phenotypic analysis. The results showed that avirulent Mtb stimulated robust immune-responses and apoptosis in macrophages to eliminate the invading Mtb; virulent Mtb induced severe necrosis and immune-escape for survival. The HMGB1 signaling pathway and TNFRSF1B plays important roles in the immune escape of virulent Mtb. Interestingly, our results suggest that macrophages kill Mtb in an IFN-{gamma} independent but simulative way, highlighting the central role of IFN signaling pathway in anti-TB immune response. Moreover, we observed selective transport of host and Mtb RNAs from macrophages to exosomes. Notably, "H37Ra-treated exosomes" displayed a higher anti-TB effect than "H37Rv-treated exosomes" due to some enriched pro-inflammation and immune-escape related Mtb proteins in these two exosomes, respectively. Conclusively, our findings shed new light on the immune mechanism of macrophages in response to Mtb infection, offering a new TB-treatment strategy and some promising vaccine candidates.

bioinformatics↗

bioRxiv2024

Longitudinal profiling of the microbiome at four body sites reveals core stability and individualized dynamics during health and disease

To understand dynamic interplay between the human microbiome and host during health and disease, we analyzed the microbial composition, temporal dynamics, and associations with host multi-omics, immune and clinical markers of microbiomes from four body sites in 86 participants over six years. We found that microbiome stability and individuality are body-site-specific and heavily influenced by the host. The stool and oral microbiome were more stable than the skin and nasal microbiomes, possibly due to their interaction with the host and environment. Also, we identified individual-specific and commonly shared bacterial taxa, with individualized taxa showing greater stability. Interestingly, microbiome dynamics correlated across body sites, suggesting systemic coordination influenced by host-microbial-environment interactions. Notably, insulin-resistant individuals showed altered microbial stability and associations between microbiome, molecular markers, and clinical features, suggesting their disrupted interaction in metabolic disease. Our study offers comprehensive views of multi-site microbial dynamics and their relationship with host health and disease. Study HighlightsO_LIThe stability of the human microbiome varies among individuals and body sites. C_LIO_LIHighly individualized microbial genera are more stable over time. C_LIO_LIAt each of the four body sites, systematic interactions between the environment, the host and bacteria can be detected. C_LIO_LIIndividuals with insulin resistance have lower microbiome stability, a more diversified skin microbiome, and significantly altered host-microbiome interactions. C_LI

microbiology↗

bioRxiv2023

Identification of a novel MCR-1 variant displaying low level of co-resistance to β-lactam antibiotics that uncovers a potential novel antimicrobial peptide

The emerging and global spread of a novel plasmid-mediated colistin resistance gene, mcr-1, threatens human health. It is accepted that MCR-1 affects bacterial fitness, and this fitness cost correlates with bacterial membrane lipid A perturbation. However, the detailed molecular mechanism remains unclear. Here, we screened out a novel MCR-1 variant, named M6, with a two-point mutation that rendered a low level of co-resistance to {beta}-lactam antibiotics. Compared to wild-type (WT) MCR-1, this variant caused severe lipid A perturbation resulting in peptidoglycan layer remodelling and thus resulted in phenotypic co-resistance to {beta}-lactams. Moreover, we found that a lipid A loading cavity is localized at the linker domain of MCR-1 and governs colistin resistance and bacterial membrane permeability, and the mutated pocket of M6 facilitates the binding affinity of lipid A. More importantly, synthetic peptides derived from M6 achieved broad-spectrum antimicrobial activity. These findings provide insights into a potential vulnerability that could be exploited in future antimicrobial drug design.

microbiology↗

bioRxiv2022

Simultaneous Profiling of Host Expression and Microbial Abundance by Spatial Meta-Transcriptome Sequencing

We developed an analysis pipeline that can extract microbial sequences from Spatial Transcriptomic (ST) data and assign taxonomic labels, generating a spatial microbial abundance matrix in addition to the default host expression matrix, enabling simultaneous analysis of host expression and microbial distribution. We called the pipeline Spatial Meta-transcriptome (SMT) and applied it on both human and murine intestinal sections and validated the spatial microbial abundance information with alternative assays. Biological insights were gained from this novel data that demonstrated host-microbe interaction at various spatial scales. Finally, we tested experimental modification that can increase microbial capture while preserving host spatial expression quality, and by use of positive controls, quantitatively demonstrated the capture efficiency and recall of our methods. This proof of concept work demonstrates the feasibility of Spatial Meta-transcriptomic analysis, and paves the way for further experimental optimization and application.

genomics↗

bioRxiv2022

Phylogeny and Metadata Network Database for Epidemiologic Surveillance

AO_SCPLOWBSTRACTC_SCPLOWThe ongoing SARS-CoV-2 pandemic has highlighted the difficulty in integrating disparate data sources for epidemiologic surveillance. To address this challenge, we have created a graph database to integrate phylogenetic trees, associated metadata, and community surveillance data for phylodynamic inference. As an example use case, we divided 22,713 SARS-CoV-2 samples into 5 groups, generated maximum likelihood trees, and inferred a potential transmission network from a forest of minimum spanning trees built on patristic distances between samples. We then used Cytoscape to visualize the resultant graphs.

evolutionary biology↗

bioRxiv2021

Spatial Meta-transcriptomes of human and murine intestines

We developed an analysis pipeline that can extract microbial sequences from Spatial Transcriptomic data and assign taxonomic labels to them, generating a spatial microbial abundance matrix in addition to the default host expression one, enabling simultaneous analysis of host expression and microbial distribution. We applied it on both human and murine intestinal datasets and validated the spatial microbial abundance information with alternative assays. Finally, we present a few biological insights that can be gained from this novel data. In summary, this proof of concept work demonstrated the feasibility of Spatial Meta-transcriptomic analysis, and pave the way for future experimental optimization.

systems biology↗

bioRxiv2021

Mapping tree species for restoration potential resilient to climate change

The restoration of forest ecosystems is associated with key benefits for biodiversity and ecosystem services. Where possible, ecosystem restoration efforts should be guided by a detailed knowledge of the native flora to regenerate ecosystems in a way that benefits natural biodiversity, ecosystem services, and natures contribution to people. Machine learning can map the ecological suitability of tree species globally, which then can guide restoration efforts, especially in regions where knowledge about the native tree flora is still insufficient. We developed an algorithm that combines ecological niche modelling and geographic distributions that allows for the high resolution (1km) global mapping of the native range and suitability of 3,987 tree species under current and future climatic conditions. We show that in most regions where forest cover could be potentially increased, heterogeneity in ecological conditions and narrow species niche width limit species occupancy, so that in several areas with reforestation potential, a large amount of potentially suitable species would be required for successful reforestation. Local tree planting efforts should consider a wide variety of species to ensure that the equally large variety of ecological conditions can be covered. Under climate change, a large fraction of the surface for restoration will suffer significant turnover in suitability, so that areas that are suitable for many species under current conditions will not be suitable in the future anymore. Such a turnover due to shifting climate is less pronounced in regions containing species with broader geographical distributions. This indicates that if restoration decisions are solely based on current climatic conditions, a large fraction of the restored area will become unsuitable in the future. Decisions on forest restoration should therefore take the niche width of a tree species into account to mitigate the risk of climate-driven ecosystem degradation.

ecology↗

bioRxiv2020

Eye-specific voluntary attention can induce a shift of perceptual ocular dominance

Ocular dominance plasticity in adults has been extensively studied in the recent decade. An interocular imbalance of visual input, e.g. monocular deprivation, has been proved to markedly reshape ocular dominance. As visual attention can be eye-specific, dissimilar visual inputs from the two eyes during monocular deprivation inevitably lead attention to be more allocated to the monocular input that conveys relatively intact information. Does the imbalanced attention across the eyes also contribute to reshaping ocular dominance? Here, using a novel "backwards-movie" adaptation paradigm, we showed that prolonged attention to the input in one eye was sufficient to shift perceptual ocular dominance in favor of the unattended eye. Furthermore, the effect was stronger when eye-specific attention was directed to the dominant eye, possibly due to fewer disturbances from the other eye during the adaptation. Taken together, these findings suggest that top-down attention plays an important role in short-term ocular dominance plasticity. Statement of RelevanceAn important goal in neuroscience is to understand and take advantage of adaptive neural plasticity. Ocular dominance plasticity resulting from imbalanced visual input signals across the two eyes has been intensively investigated. By developing a novel "backwards-movie" paradigm in which movie images played normally were presented to one eye while movie images of the same episode but played backwards were presented to the other eye, the current study for the first time demonstrates the non-negligible contributions of selective attention in reshaping ocular dominance. These findings expand the homeostatic compensation theory of monocular deprivation by highlighting the contributions of feedback signals. Furthermore, our method could be applied in future work to explore new possibilities in treating adults with amblyopia.

neuroscience↗

bioRxiv2019

Molecular Networks and Key Regulators of the Dysregulated Neuronal System in Alzheimer’s Disease

To study the molecular mechanisms driving the pathogenesis and identify novel therapeutic targets of late onset Alzheimers Disease (LOAD), we performed an integrative network analysis of whole-genome DNA and RNA sequencing profiling of four cortical areas, including the parahippocampal gyrus, across 364 donors spanning the full spectrum of LOAD-related cognitive and neuropathological disease severities. Our analyses revealed thousands of molecular changes and uncovered for the first-time multiple neuron specific gene subnetworks most dysregulated in LOAD. ATP6V1A, a critical subunit of vacuolar-type H+-ATPase (v-ATPase), was predicted to be a key regulator of one neuronal subnetwork and its role in disease-related processes was evaluated through CRISPR-based manipulation of human induced pluripotent stem cell derived neurons and RNAi-based knockdown in transgenic Drosophila models. This study advances our understanding of LOAD pathogenesis by providing the global landscape and detailed circuits of complex molecular interactions and regulations in several key brain regions affected by LOAD and the resulting network models provide a blueprint for developing next generation therapeutics against LOAD.

neuroscience↗

bioRxiv2019

Chromosome level draft genomes of the fall armyworm, Spodoptera frugiperda (Lepidoptera: Noctuidae), an alien invasive pest in China

The fall armyworm (FAW), Spodoptera frugiperda (J.E. Smith) is a severely destructive pest native to the Americas, but has now become an alien invasive pest in China, and causes significant economic loss. Therefore, in order to make effective management strategies, it is highly essential to understand genomic architecture and its genetic background. In this study, we assembled two chromosome scale genomes of the fall armyworm, representing one male and one female individual procured from Yunnan province of China. The genome sizes were identified as 542.42 Mb with N50 of 14.16 Mb, and 530.77 Mb with N50 of 14.89 Mb for the male and female FAW, respectively. We predicted about 22,201 genes in the male genome. We found the expansion of cytochrome P450 and glutathione s-transferase gene families, which are functionally related to the intensified detoxification and pesticides tolerance. Further population analyses of corn strain (C strain) and rice strain (R strain) revealed that the Chinese fall armyworm was most likely invaded from Africa. These strain information, genome features and possible invasion source described in this study will be extremely important for making effective strategies to manage the fall armyworms.

genomics↗

bioRxiv2018

MiRNA expression profiles of serum exosomes derived from individuals with latent and active tuberculosis

Tuberculosis (TB) has become a leading cause of death worldwide, which is largely attributed to the difficulties in diagnosis and treatment of TB patients. Exosomes carrying RNA, particularly miRNA, have been indicated their functional and diagnostic potential in diseases, including tuberculosis (TB). In the present study, we performed RNA-seq based analysis on exosomal miRNA profiles for clinical specimens of healthy controls (HC), active tuberculosis (TB) and latent tuberculosis infection (LTBI). We identified many distinct up-regulated and down-regulated differentially expressed miRNA and further screened top 20 in each compared groups which might provide a potential panel for differentiation of HC, LTBI, and TB. We classified all the differentially expressed miRNAs into six expression patterns and identified three persistently up-regulated miRNA (hsa-miR-140-3p, hsa-miR-3184-5p and hsa-miR-423-3p) as potential markers during TB progression. Combined with our previously detected exsomal mRNA, we screened the genes overlapped with predicted mRNA targets of differentially expressed miRNA and analyzed their involvement in Biological Process, indicating a decreased signaling transduction and increased cell death in LTBI and TB. Our results indicate the selective packaging of RNA cargoes into exosomes under different stages of Mycobacterium tuberculosis infection and facilitate further study of TB pathogenesis and development.\n\nIMPORTANCEThe main reason for failure to eliminate TB is lack of understanding molecular mechanism of TB pathogenesis and difficulties in TB diagnosis and treatment. Exosomes provide a promising research tool because they are released from various cells containing valuable biochemical information related to diseases. We reveale distinct miRNA expression profile of the exosomes, which indicates selective packaging of RNA cargoes into exosomes under different stages of Mycobacterium tuberculosis infection. Further, we also provide evidence of related miRNA candidates potentially involving in TB progression and facilitating discovery of TB biomarkers.

microbiology↗