Biology subjects

Le, T. T.

Publications and source records attributed to Le, T. T..

At least 19 recordsLinked to original sources

bioRxiv2026

Urban Vietnam at the microbiome transition: Co-existing enterotypes reflect the global industrialization patterns

Vietnam's rapid socioeconomic and dietary transition offers a rare window into how industrialization is reflected in the gut microbiome, yet Vietnamese populations remain underrepresented in global reference datasets. We investigated whether healthy Vietnamese adults in Hanoi harbor microbial community configurations associated with different stages of industrialization. Metagenomic data from stool samples of 183 clinically screened participants in Hanoi were analyzed alongside 629 publicly available metagenomic datasets from populations in low to middle income (LMI) and high income (HI) countries. Species-level taxonomic composition and gene-content-based metabolic pathways were characterized using community clustering and multivariable association analyses. Rather than forming a single population profile, the Vietnamese cohort separated into two enterotypes that mirrored the global industrialization gradient. Enterotype 1 more closely resembled populations from LMICs and showed greater microbial richness and diversity, whereas Enterotype 2 aligned with taxonomic and functional profiles observed in HICs. Both taxonomic and functional potential shows similar trajectories. Diet and lifestyle patterns describe some of the variance between enterotypes, supporting an association between contemporary exposures and microbiome structure without establishing causation. Antibiotic resistance profiles also varied between enterotypes, suggesting that the transition may encompass functions relevant to antimicrobial exposure. Together, these findings position urban Vietnam at a microbiome transition, where community states associated with different levels of industrialization coexist within a single population. This Vietnamese reference cohort expands representation in global metagenomic research and provides a baseline for tracking how rapid socioeconomic change may reshape microbial ecology, metabolic capacity, and antimicrobial resistance.

microbiology↗

bioRxiv2025

Triple-Negative Breast Cancer Cells Activate Sensory Neurons via TRPV1 to Drive Nerve Outgrowth and Tumor Progression

The tumor microenvironment in triple-negative breast cancer (TNBC) is characterized by increased sensory nerve density, which contributes to cancer progression by promoting migration and metastasis. However, the origin of tumor-innervating nerves and the mechanisms driving sensory innervation into tumors remain poorly understood. Using in vivo retrograde labeling techniques, we show that mammary tumors are associated with an increase in nerves originating from the dorsal root ganglia. Additionally, we find that TNBC cells trigger stress and activation markers and induce neuronal firing in a transient receptor potential anilloid subtype 1 (TRPV1)-dependent manner. In both 2D and 3D cell culture models, TNBC cells promote outgrowth of sensory nerves that is abrogated with Trpv1 knockout. We identified c-Jun and IL-6 as an effector of neurite outgrowth that acts downstream of TRPV1 to promote outgrowth in vitro. Finally, in Trpv1 knockout mice, TNBC tumors exhibit delayed growth and reduced lung metastasis. These findings suggest that a critical role for TRPV1 in tumor-nerve crosstalk, offering a potential target to reduce metastatic disease.

cancer biology↗

bioRxiv2025

Cinnamomum cassia Extract and Its Novel Isolated Compound Suppress Inflammation via Autophagy Induction in Sepsis

Uncontrolled inflammation is central to the development of diseases such as sepsis, and autophagy has emerged as a critical regulatory mechanism in this process. The ethanol extract of Cinnamomum cassia (EECC) was identified as a potent autophagy inducer through high-throughput LC3 reporter screening. EECC enhanced autophagic flux, as confirmed by RFP-GFP-LC3 imaging and immunoblotting. It also suppressed Toll-like receptor signaling and reduced pro-inflammatory cytokine production in macrophages. EECC inhibited nuclear factor-{kappa}B signaling in an autophagy-dependent manner, as this effect was reversed by autophagy inhibitors. To identify active constituents, 24 compounds were isolated from EECC, including six novel structures. Among the novel compounds, Cassitamine F exhibited dual activity as an autophagy inducer and inflammation suppressor. In a lipopolysaccharide-induced sepsis model, Cassitamine F significantly reduced serum levels of pro-inflammatory cytokines. These findings suggest that EECC and Cassitamine F may hold therapeutic potential for autophagy-targeted treatment of sepsis and other inflammation-related disorders. Highlights- Ethanol extract of Cinnamomum cassia (EECC) identified as a potent autophagy inducer via high-throughput LC3 HiBiT screening. - EECC suppresses Toll-like receptor signaling and pro-inflammatory cytokines through autophagy-dependent pathways. - Twenty-four compounds were isolated from EECC, including six novel structures (Cassitamine A-F). - Cassitamine F exhibits dual activity: induction of autophagy and inhibition of inflammation. - Cassitamine F significantly reduces serum cytokine levels in an LPS-induced sepsis model, suggesting therapeutic potential.

pharmacology and toxicology↗

bioRxiv2025

β-nicotinamide mononucleotide production in Vibrio natriegens: a preliminary study

BackgroundNicotinamide mononucleotide (NMN), is a promising nutraceutical attracting much attention for its pharmacological and anti-aging efficacies. However, NMN-containing commercial products are very high-priced due to the lack of efficient and facile methods for industrial-scale production. To date, various metabolic engineering strategies have been successfully applied to produce NMN in Escherichia coli. Recently, Vibrio natriegens has become a promising host in the bioindustry thanks to its rapid growth and capabilities of broad substrate utilization. This study aims to evaluate the NMN biosynthesis capability of V. natriegens. MethodsFirstly, a mutant V. natriegens strain ({Delta}dns::araC-T7RNAP-KanR{Delta} pncC::FtnadE-SmR{Delta} nadR) was generated via multiplex genome editing by natural transformation (MuGENT). Nampt genes encoding nicotinamide phosphoribosyltransferase from Chitinophaga pinensis, Sphingopyxis sp. C-1, Haemophilus ducreyi, and Vibrio phage KVP40 were codon-optimized and cloned into pACYCDuet-1 under the control of T7 promoter. The recombinant plasmids were electroporated into the mutant strain. The expression of recombinant NAMPTs in V. natriegens was evaluated by SDS-PAGE analysis and the intracellular NMN concentrations were quantified by HPLC. ResultsAfter two rounds of MuGENT, V. natriegens V54-33 strain ({Delta}dns::araC-T7RNAP-KanR{Delta} pncC::FtnadE-SmR{Delta} nadR) was successfully generated. SDS-PAGE analysis demonstrated that all NAMPTs were strongly expressed in the V54-33 strain. HPLC analysis revealed that the highest intracellular NMN concentration was obtained with NAMPT from Chitinophaga pinensis (44.5 M), followed by NAMPT from Vibrio phage KVP40 (23.3 M). ConclusionThis study demonstrated the feasibility of NMN biosynthesis in V. natriegens.

bioengineering↗

bioRxiv2024

RNA Polymerase II is a Polar Roadblock to a Progressing DNA Fork

DNA replication and transcription occur simultaneously on the same DNA template, leading to inevitable conflicts between the replisome and RNA polymerase. These conflicts can stall the replication fork and threaten genome stability. Although numerous studies show that head-on conflicts are more detrimental and more prone to promoting R-loop formation than co-directional conflicts, the fundamental cause for the RNA polymerase roadblock polarity remains unclear, and the structure of these R-loops is speculative. In this work, we use a simple model system to address this complex question by examining the Pol II roadblock to a DNA fork advanced via mechanical unzipping to mimic the replisome progression. We found that the Pol II binds more stably to resist removal in the head-on configuration, even with minimal transcript size, demonstrating that the Pol II roadblock has an inherent polarity. However, an elongating Pol II with a long RNA transcript becomes an even more potent and persistent roadblock while retaining the polarity, and the formation of an RNA-DNA hybrid mediates this enhancement. Surprisingly, we discovered that when a Pol II collides with the DNA fork head-on and becomes backtracked, an RNA-DNA hybrid can form on the lagging strand in front of Pol II, creating a topological lock that traps Pol II at the fork. TFIIS facilitates RNA-DNA hybrid removal by severing the connection of Pol II with the hybrid. We further demonstrate that this RNA-DNA hybrid can prime lagging strand replication by T7 DNA polymerase while Pol II is still bound to DNA. Our findings capture basal properties of the interactions of Pol II with a DNA fork, revealing significant implications for transcription-replication conflicts.

biophysics↗

bioRxiv2024

An Effective Surface Passivation Assay for Single-Molecule Studies of Chromatin and Topoisomerase II

For single-molecule studies requiring surface anchoring of biomolecules, a poorly passivated surface can result in alterations of biomolecule structure and function that can result in artifacts. This protocol describes surface passivation and sample chamber preparation for mechanical manipulation of chromatin fibers and characterization of topoisomerase II activity in physiological buffer conditions. The method employs enhanced surface hydrophobicity and purified blocking proteins to reduce non-specific surface adsorption. This method is accessible, cost-effective, and potentially widely applicable to other biomolecules. For a complete list of publications that employ this protocol, see the paper references. B. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=154 SRC="FIGDIR/small/614989v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@d52b73org.highwire.dtl.DTLVardef@117bfc3org.highwire.dtl.DTLVardef@2eb670org.highwire.dtl.DTLVardef@cb88b2_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

bioRxiv2024

Tensor Kernel Learning for Classification of Alzheimer's Conditions using Multimodal Data

Early, timely, and accurate assessment of Alzheimers disease (AD), particularly at its earlier stage - mild cognitive impairment (MCI) -, is central to detecting, managing, and potentially treating the disease. The biological underpinnings of AD, however, is multifaceted, from genetic variations, abnormal protein accumulation, to irregular brain functions and structure. A joint analysis of these data, therefore, may offer potentially new insights about AD-related biomarkers and AD prediction. But such explorations must confront the complexity of these data: heterogeneity, multimodality and high-dimensionality. Here, to address these challenges, we propose a new machine-learning method, namely the tensor kernel learning (TKL), leveraging tensor methods and kernel learning, to enhance AD assessment by enhancing multi-modal data integration. More specifically, TKL first uses CP/PARAFAC decomposition and graph diffusion to fuse multiple kernels learned from four complementary data modalities (MRI, PET, CSF, and SNP data). We then used a supervised kernel for a kernel SVM classifier to identify potential patients. To evaluate the effectiveness of TKL, we apply it to data from the Alzheimers Disease Neuroimaging Initiative (ADNI; the sample size n = 331 subjects), including cognitively normal individuals (CN), MCI subjects, and AD patients. TKL improves AD classification performance in both linear and nonlinear combinations, achieving accuracies of 91.31% for CN vs. AD, 81.45% for CN vs. MCI, and 78.27% for AD vs. MCI, compared to 85.48%, 70.89%, and 73.51% using the best single modality. Additionally, TKL reveals clearer, more structured patterns in the data, enhancing interpretation and understanding of the relationships among different modalities. Detailed implementation details of our method can be found at: https://github.com/thanhvd18/Tensor-Kernel-Learning-matlab.

neuroscience↗

bioRxiv2023

Cell morphology best predicts tumorigenicity and metastasis in vivo across multiple TNBC cell lines of different metastatic potential

BackgroundMetastasis is the leading cause of death in breast cancer patients. For metastasis to occur, tumor cells must invade locally, intravasate, and colonize distant tissues and organs, all steps that require tumor cell migration. The majority of studies on invasion and metastasis rely on human breast cancer cell lines. While it is known that these cells have different properties and abilities for growth and metastasis, the in vitro morphological, proliferative, migratory, and invasive behavior of these cell lines and their correlation to in vivo behavior is poorly understood. Thus, we sought to classify each cell line as poorly or highly metastatic by characterizing tumor growth and metastasis in a murine model of six commonly used human triple-negative breast cancer xenografts, as well as determine which in vitro assays commonly used to study cell motility best predict in vivo metastasis. MethodsWe evaluated the liver and lung metastasis of human TNBC cell lines MDA-MB-231, MDA-MB-468, BT549, Hs578T, BT20, and SUM159 in immunocompromised mice. We characterized each cell lines cell morphology, proliferation, and motility in 2D and 3D to determine the variation in these parameters between cell lines. ResultsWe identified MDA-MB-231, MDA-MB-468, and BT549 cells as highly tumorigenic and metastatic, Hs578T as poorly tumorigenic and metastatic, BT20 as intermediate tumorigenic with poor metastasis to the lungs but highly metastatic to the livers, and SUM159 as intermediate tumorigenic but poorly metastatic to the lungs and livers. We showed that metrics that characterize cell morphology are the most predictive of tumor growth and metastatic potential to the lungs and liver. Further, we found that no single in vitro motility assay in 2D or 3D significantly correlated with metastasis in vivo. ConclusionsOur results provide an important resource for the TNBC research community, identifying the metastatic potential of 6 commonly used cell lines. Our findings also support the use of cell morphological analysis to investigate the metastatic potential and emphasize the need for multiple in vitro motility metrics using multiple cell lines to represent the heterogeneity of metastasis in vivo.

cancer biology↗

bioRxiv2021

Passage of SARS-CoV-2 in cells expressing human and mouse ACE2 selects for mouse-adapted and ACE2-independent viruses

Human ACE2 (hACE2) is the key cell attachment and entry receptor for SARS-CoV-2, with the original SARS-CoV-2 isolates unable to use mouse ACE2 (mACE2). Herein we describe a new system for generating mouse-adapted SARS-CoV-2 in vitro by serial passaging virus in co-cultures of cell lines expressing hACE2 and mACE2. Mouse-adapted viruses emerged with up to five amino acid changes in the spike protein, all of which have been seen in human isolates. Mouse-adapted viruses replicated to high titers in C57BL/6J mouse lungs and nasal turbinates, and caused severe lung histopathology. One mouse-adapted virus was also able to replicate efficiently in ACE2-negative cell lines, with ACE2-independent entry by SARS-CoV-2 representing a new biology for SARS-CoV-2 that has potential widespread implications for disease and intervention development.

microbiology↗

bioRxiv2021

Comparative genomics of Acinetobacter baumannii and therapeutic bacteriophages from a patient undergoing phage therapy

In 2016, a 68-year-old patient with a disseminated multi-drug resistant Acinetobacter baumannii infection was treated using lytic bacteriophages in one of the first modern human clinical uses of phage therapy in the United States. Due to the emergency nature of the treatment there was little time to thoroughly characterize the phages used in this intervention or the pathogen itself. Here we report the genomes of the nine phages used for treatment and three strains of A. baumannii isolated prior to and during treatment. The eight phages used in the initial treatment were found to be a group of closely related T4-like myophages; the ninth phage, AbTP3{Phi}1, was found to be an unrelated Fri1-like podophage. Analysis of 19 A. baumannii isolates collected before and during phage treatment showed that resistance to the T4-like phages appeared as early as two days following the start of treatment. Three A. baumannii strains (TP1, TP2 and TP3) collected before and during treatment were sequenced to closure, and all contained a 3.9 Mb chromosome of sequence type 570 with a KL116 capsule locus and identical 8.7 kb plasmids. Phage-insensitive mutants of A. baumannii strain TP1 were generated in vitro and the majority of identified mutations were located in the bacterial capsule locus. The presence of the same mutation in both the in vitro mutants and in phage-insensitive isolates TP2 and TP3, which evolved in vivo during phage treatment, indicate that in vitro investigations can produce results that are relevant and predictive for the in vivo environment.

microbiology↗

bioRxiv2021

Sensory nerves enhance triple-negative breast cancer migration and metastasis via the axon guidance molecule PlexinB3

In breast cancer, nerve presence has been correlated with more invasive disease and worse prognosis, yet the mechanisms by which different types of peripheral nerves drive tumor progression remain poorly understood. In this study, we identified sensory nerves as more abundant in human triple-negative breast cancer (TNBC) tumors. Coinjection of sensory neurons isolated from the dorsal root ganglia (DRG) of adult female mice with human TNBC cells in immunocompromised mice increased the number of lung metastases. Direct in vitro co-culture of human TNBC cells with the dorsal root ganglia (DRG) of adult female mice revealed that TNBC cells adhere to sensory neuron fibers leading to an increase in migration speed. Species-specific RNA sequencing revealed that co-culture of TNBC cells with sensory nerves upregulates the expression of genes associated with cell migration and adhesion in cancer cells. We demonstrate that the axon guidance molecule Plexin B3 mediates cancer cell adhesion to and migration on sensory nerves. Together, our results identify a novel mechanism by which nerves contribute to breast cancer migration and metastasis by inducing a shift in TNBC cell gene expression and support the rationale for disrupting neuron-cancer cell interactions to target metastasis. SignificanceThe presence of nerves in breast tumors has been associated with poor outcome. Understanding the mechanisms by which nerves contribute to tumor progression could help identify novel strategies to target metastatic disease.

cancer biology↗

bioRxiv2021

Microplastic consumption induces inflammatory signatures in the colon and prolongs a viral arthritis

Global microplastic (MP) contamination and the effects on the environment are well described. However, the potential for MP consumption to affect human health remains controversial. Mice consuming {approx}80 {micro}g/kg/day of 1 {micro}m polystyrene MPs via their drinking water for a month showed no weight loss, nor were MPs detected in organs. The microbiome was also unchanged. MP consumption did lead to small transcriptional changes in the colon suggesting plasma membrane perturbations and mild inflammation. Mice were challenged with the arthritogenic chikungunya virus, with MP consumption leading to a significantly prolonged arthritic foot swelling that was associated with elevated Th1, NK cell and neutrophil signatures. Immunohistochemistry also showed a significant increase in the ratio of neutrophils to monocyte/macrophages. The picture that emerges is reminiscent of enteropathic arthritis, whereby perturbations in the colon are thought to activate innate lymphoid cells that can inter alia migrate to joint tissues to promote inflammation.

immunology↗

bioRxiv2021

Potassium channel-driven bioelectric signaling regulates metastasis in triple-negative breast cancer

There is a critical need to better understand the mechanisms that drive local cell invasion and metastasis to develop new therapeutics targeting metastatic disease. Bioelectricity is an important mediator of cellular processes and changes in the resting membrane potential (RMP) are associated with increased cancer cell invasion. However, the mechanism is not well understood. Our data demonstrate that altering the RMP of triple-negative breast cancer (TNBC) cells by manipulating potassium channel expression increases in vitro invasion, in vivo tumor growth, and metastasis, and is accompanied by changes in gene expression associated with cell adhesion. We describe a novel mechanism for RMP-mediated cell migration involving cadherin-11 and the MAPK pathway. Importantly, we identify a new strategy to target metastatic TNBC in vivo by repurposing FDA-approved potassium channel blockers. Our results provide an understanding of the mechanisms by which bioelectricity regulates cancer cell invasion and metastasis that could lead to a new class of therapeutics for patients with metastatic disease.

cancer biology↗

bioRxiv2021

Genetic analysis of coronary artery disease using tree-based automated machine learning informed by biology-based feature selection

Machine Learning (ML) approaches are increasingly being used in biomedical applications. Important challenges of ML include choosing the right algorithm and tuning the parameters for optimal performance. Automated ML (AutoML) methods, such as Tree-based Pipeline Optimization Tool (TPOT), have been developed to take some of the guesswork out of ML thus making this technology available to users from more diverse backgrounds. The goals of this study were to assess applicability of TPOT to genomics and to identify combinations of single nucleotide polymorphisms (SNPs) associated with coronary artery disease (CAD), with a focus on genes with high likelihood of being good CAD drug targets. We leveraged public functional genomic resources to group SNPs into biologically meaningful sets to be selected by TPOT. We applied this strategy to data from the UK Biobank, detecting a strikingly recurrent signal stemming from a group of 28 SNPs. Importance analysis of these uncovered functional relevance of the top SNPs to genes whose association with CAD is supported in the literature and other resources. Furthermore, we employed game-theory based metrics to study SNP contributions to individual level TPOT predictions and discover distinct clusters of well-predicted CAD cases. The latter indicates a promising approach towards precision medicine.

bioinformatics↗

bioRxiv2021

RNA-sequencing indicates immune cell signaling and inflammatory gene expression in cardiac fibroblasts increases with developmental age

BackgroundCardiac fibroblasts are responsible for extracellular matrix turnover and repair in the cardiac environment and serve to help facilitate immune responses. However, it is well established that they have significant phenotypic heterogeneity with respect to location, physiological conditions, and developmental age. The goal of this study was to provide an in-depth transcriptomic profile of cardiac fibroblasts derived from rat hearts at fetal, neonatal, and adult developmental ages to ascertain variations in gene expression that may drive functional differences in these cells at these specific stages of development. ResultsWe performed RNA-seq of cardiac fibroblasts isolated from fetal, neonatal, and adult rats was performed and compared to the rat genome. Principal component analysis of RNA-seq data suggested data variance was predominantly due to developmental age. Differential expression and Gene set enrichment analysis against Gene Ontology and Kyoto Encyclopedia of Genes and Genomes datasets indicated an array of differences across developmental ages, including significant decreases in cardiac development and cardiac function-associated genes with age, and a significant increase in immune and inflammatory-associated functions - particularly immune cell signaling, and cytokine and chemokine production - with respect to increasing developmental age. ConclusionThese results reinforce established evidence of diverse phenotypic heterogeneity of fibroblasts with respect to developmental age. Further, based on our analysis of gene expression, age-specific alterations in cardiac fibroblasts may play a crucial role in observed differences in cardiac inflammation and immune response observed across developmental ages.

cell biology↗

bioRxiv2021

SARS-CoV-2 infection models using in vivo and in vitro hACE2-lentivirus transduction

SARS-CoV-2 uses the human ACE2 (hACE2) receptor for cell attachment and entry, with mouse ACE2 (mACE2) unable to support infection. Herein we describe an ACE2-lentivirus system and illustrate its utility for in vitro and in vivo SARS-CoV-2 infection models. Transduction of non-permissive cell lines with hACE2 imparted replication competence, and transduction with mACE2 containing N30D, N31K, F83Y and H353K substitutions, to match hACE2, rescued SARS-CoV-2 replication. Intranasal hACE2-lentivirus transduction of C57BL/6J mice permitted significant virus replication in lungs. RNA-Seq analyses illustrated that the model involves an acute inflammatory disease followed by resolution and tissue repair, with a transcriptomic profile similar to that seen in COVID-19 patients. Intranasal hACE2-lentivirus transduction of IFNAR-/- and IL-28RA-/- mice lungs was used to illustrate that loss of type I or III interferon responses have no significant effect on virus replication. However, their importance in driving inflammatory responses was illustrated by RNA-Seq analyses. We also demonstrate the utility of the hACE2-lentivirus transduction system for vaccine evaluation in C57BL/6J mice. The ACE2-lentivirus system thus has broad application in SARS-CoV-2 research, providing a tool for both mutagenesis studies and mouse model development. AUTHOR SUMMARYSARS-CoV-2 uses the human ACE2 (hACE2) receptor to infect cells, but cannot infect mice because the virus cannot bind mouse ACE2 (mACE2). We use an ACE2-lentivirus system in vitro to identify four key amino acids in mACE2 that explain why SARS-CoV-2 cannot infect mice. hACE2-lentivirus was used to express hACE2 in mouse lungs in vivo, with the inflammatory responses after SARS-CoV-2 infection similar to those seen in human COVID-19. Genetically modified mice were used to show that type I and III interferon signaling is required for the inflammatory responses. We also show that the hACE2-lentivirus mouse model can be used to test vaccines. Overall this paper demonstrates that our hACE2-lentivirus system has multiple applications in SARS-CoV-2 and COVID-19 research.

microbiology↗

bioRxiv2020

Systems vaccinology analysis of a recombinant vaccinia-based vector reveals diverse innate immune signatures at the injection site

Poxvirus systems have been extensively used as vaccine vectors. Herein a systems vaccinology analysis of intramuscular injection sites provides detailed insights into host innate immune responses, as well as expression of vector and recombinant immunogen genes, after vaccination with a new multiplication defective, vaccinia-based vector, Sementis Copenhagen Vector. Chikungunya and Zika virus immunogen mRNA and protein expression was associated with necrosing skeletal muscle cells surrounded by mixed cellular infiltrates. Adjuvant signatures at 12 hours post-vaccination were dominated by TLR3, 4 and 9, STING, MAVS, PKR and the inflammasome. Th1 cytokine signatures were dominated by IFN{gamma}, TNF and IL1{beta}, and chemokine signatures by CCL5 and CXCL12. Multiple signatures associated with dendritic cell stimulation were evident. By day seven, vaccine transcripts were absent, and cell death, neutrophil, macrophage and inflammation annotations had abated. No compelling arthritis signatures were identified. Such innate systems vaccinology approaches should inform refinements in poxvirus-based vector design.

systems biology↗

bioRxiv2020

Analysis of ISCB honorees and keynotes reveals disparities

Delivering a keynote talk at a conference organized by a scientific society, or being named as a fellow by such a society, indicates that a scientist is held in high regard by their colleagues. To explore if the distribution of such indicators of esteem in the field of bioinformatics reflects the composition of this field, we compared the gender, name-origin, country of affiliation and race/ethnicity of 412 researchers who had been recognized by the International Society for Computational Biology (75 fellows and 337 keynote speakers) with over 170,000 researchers who had been the last authors on computational biology papers between 1993 and 2019. The proportion of female fellows and keynote speakers was similar to that of the field overall. However, names of East Asian origin have been persistently underrepresented among fellows and keynote speakers. Moreover, fellows and keynote speakers with an affiliation in the United States were overrepresented by a factor of 2.1; almost two thirds of this excess was accounted for by a deficit of 101 fellows and keynote authors from China, India, France and Italy. Within the US, we found an excess of white fellows and keynote speakers and a depletion of Asian fellows and keynote speakers.

bioinformatics↗