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Biology subjects

Zhou, Z.

Publications and source records attributed to Zhou, Z..

At least 361 records · Page 20Linked to original sources

Distributed representations for human inference

Inferring relationships that go beyond our direct experience is essential for understanding our environment. This capacity requires either building representations that directly reflect structure across experiences as we encounter them, or computing the indirect relationships across experiences as the need arises. Building structure directly into overlapping representations allows for powerful learning and generalization in neural network models, but building these so-called distributed representations requires inputs to be encountered in interleaved order. We test whether interleaving similarly facilitates the formation of representations that directly integrate related experiences in humans, and what advantages such integration may confer for behavior. In a series of behavioral experiments, we present evidence that interleaved learning indeed promotes the formation of representations that directly link across related experiences. As in neural network models, interleaved learning gives rise to fast and automatic recognition of item relatedness, affords efficient generalization, and is especially critical for inference when learning requires statistical integration of noisy information over time. We use the data to adjudicate between several existing computational models of human memory and inference. The results demonstrate the power of interleaved learning and implicate the formation of integrated, distributed representations that support generalization in humans.

neuroscience↗

Photosensitized Electrospun Nanofibrous Filters for Capturing and Killing Airborne Coronaviruses under Visible Light Irradiation

To address the challenge of the airborne transmission of SARS-CoV-2, photosensitized electrospun nanofibrous membranes were fabricated to effectively capture and inactivate coronavirus aerosols. With an ultrafine fiber diameter ([~] 200 nm) and a small pore size ([~] 1.5 {micro}m), the optimized membranes caught 99.2% of the aerosols of the murine hepatitis virus A59 (MHV-A59), a coronavirus surrogate for SARS-CoV-2. In addition, rose bengal was used as the photosensitizer for the membranes because of its excellent reactivity in generating virucidal singlet oxygen, and the membranes rapidly inactivated 98.9% of MHV-A59 in virus-laden droplets only after 15 min irradiation of simulated reading light. Singlet oxygen damaged the virus genome and impaired virus binding to host cells, which elucidated the mechanism of disinfection at a molecular level. Membrane robustness was also evaluated, and no efficiency reduction for filtering MHV-A59 aerosols was observed after the membranes being exposed to both indoor light and sunlight for days. Nevertheless, sunlight exposure photobleached the membranes, reduced singlet oxygen production, and compromised the performance of disinfecting MHV-A59 in droplets. In contrast, the membranes after simulated indoor light exposure maintained their excellent disinfection performance. In summary, photosensitized electrospun nanofibrous membranes have been developed to capture and kill airborne environmental pathogens under ambient conditions, and they hold promise for broad applications as personal protective equipment and indoor air filters. SynopsisPhotosensitized electrospun nanofibrous filters with excellent capture-and-kill performance against coronaviruses were designed and implemented to prevent the airborne transmission of COVID-19. Table of Contents O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=103 SRC="FIGDIR/small/454404v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@171d6corg.highwire.dtl.DTLVardef@18caad5org.highwire.dtl.DTLVardef@23b902org.highwire.dtl.DTLVardef@14746e4_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

The swine spatiotemporal H3K27ac spectrum provides novel resources for exploring gene regulation related to complex traits and fundamental biological process

The limited knowledge of genomic non-coding and regulatory regions has limited our ability to decipher the genetic mechanisms underlying complex traits in pigs. In this study, we characterize the spatiotemporal landscape of putative enhancers and promoters and their target genes by combining H3K27ac targeted ChIP-Seq and RNA-Seq in fetal (day 74-75 pc) and adult (day 132-150 pn) tissues (brain, liver, heart, muscle and small intestine) sampled from Asian aboriginal Bamaxiang and European highly selected Large White pigs of both sexes. We identify 101,290 H3K27ac peaks marking 18,521 promoters and 82,769 enhancers, including peaks that are active across all tissues and developmental stages could indicate safe harbors for exogenous gene insertion, and tissue and developmental-stage specific peaks that regulate genes pathways matching tissue and developmental stage specific physiological functions. We found H3K27ac and DNA methylation in the promoter region of the XIST gene may involve in X chromosome inactivation, and demonstrate utility of the present resource to reveal regulatory patterns of known causal genes and to prioritize candidate causal variants for complex traits in pigs. We have developed a web browser to improve the accessibility of the results (http://39.108.231.116/browser/?genome=susScr11).

genomics↗

Molecular Pathophysiology of Cardiac Injury and Cardiac Microthrombi in Fatal COVID-19: Insights from Clinico-histopathologic and Single Nuclei RNA Sequencing Analyses

Cardiac injury is associated with critical COVID-19, yet its etiology remains debated. To elucidate the pathogenic mechanisms of COVID-19-associated cardiac injury, we conducted a single-center prospective cohort study of 69 COVID-19 decedents. Of six cardiac histopathologic features, microthrombi was the most commonly detected (n=48, 70%). We tested associations of cardiac microthrombi with biomarkers of inflammation, cardiac injury, and fibrinolysis and with in-hospital antiplatelet therapy, therapeutic anticoagulation, and corticosteroid treatment, while adjusting for multiple clinical factors, including COVID-19 therapies. Higher peak ESR and CRP during hospitalization were independently associated with higher odds of microthrombi. Using single nuclei RNA-sequence analysis, we discovered an enrichment of pro-thrombotic/anti-fibrinolytic, extracellular matrix remodeling, and immune-potentiating signaling amongst cardiac fibroblasts in microthrombi-positive COVID-19 hearts relative to microthrombi-negative COVID-19. Non-COVID-19 non-failing hearts were used as reference controls. Our cumulative findings identify the specific transcriptomic changes in cardiac fibroblasts as salient features of COVID-19-associated cardiac microthrombi.

pathology↗

Lineage-specific regulatory changes in the pathological cardiac remodeling of hypertrophy cardiomyopathy unraveled by single-nucleus RNA-seq and spatial transcriptomics

BACKGROUNDHypertrophy cardiomyopathy (HCM) is the most common cardiac genetic disorder with the histopathological features of cardiomyocyte hypertrophy and cardiac fibrosis. The pathological remodeling that occurs in the myocardium of HCM patients may ultimately progress to heart failure and death. A thorough understanding of the cell type-specific changes in the pathological cardiac remodeling of HCM is crucial for developing successful medical therapies to prevent or mitigate the progression of this disease. METHODSWe performed single-nucleus RNA-seq of the cardiac tissues from 10 HCM patients and 2 healthy donors, and conducted spatial transcriptomic assays of 4 cardiac tissue sections from 3 HCM patients. Comparative analyses were performed to explore the lineage-specific changes in expression profile, subpopulation composition and intercellular communication in the cardiac tissues of HCM patients. Based on the results of independent analyses including pseudotime ordering, differential expression analysis, and differential regulatory network analysis, we prioritized candidate therapeutic targets for mitigating the progression to heart failure or attenuating the cardiac fibrosis in HCM. Using the spatial transcriptomic data, we examined the spatial activity patterns of the key candidate genes, pathways and subpopulations. RESULTSUnbiased clustering of 55,122 nuclei from HCM and healthy conditions revealed 9 cell lineages and 28 clusters. Significant expansion of vascular-related lineages and contraction of cardiomyocytes, fibroblasts and myeloid cells in HCM were observed. The transcriptomic dynamics during the transition towards the failing state of cardiomyocytes in HCM were uncovered. Candidate target genes for mitigating the progression to heart failure in HCM were obtained such as FGF12, IL31RA, BDNF, S100A1, CRYAB and PROS1. The transcriptomic dynamics underlying the fibroblast activation were also uncovered, and candidate targets for attenuating the cardiac fibrosis in HCM were obtained such as RUNX1, MEOX1, AEBP1, LEF1 and NRXN3. CONCLUSIONSWe provided a comprehensive analysis of the lineage-specific regulatory changes in HCM. Our analysis identified a vast array of candidate therapeutic target genes and pathways to prevent or attenuate the pathological remodeling of HCM. Our datasets constitute a valuable resource to examine the lineage-specific expression changes of HCM at single-nucleus and spatial resolution. We developed a web-based interface (http://snsthcm.fwgenetics.org/) for further exploration.

pathology↗

Autophagosomes fuse to phagosomes and play important roles in the degradation of apoptotic cells in Caenorhabditis elegans

Autophagosomes are double-membrane intracellular vesicles that degrade protein aggregates, intracellular organelles, and other cellular components. During the development of the nematode Caenorhabditis elegans, many somatic and germ cells undergo apoptosis. These cells are engulfed and degraded by their neighboring cells. We discovered a novel role of autophagosomes in facilitating the degradation of apoptotic cells using a real-time imaging technique. Specifically, the double-membrane autophagosomes in engulfing cells are recruited to the surfaces of phagosomes containing apoptotic cells and subsequently fuse to phagosomes, allowing the inner vesicle to enter the phagosomal lumen. Mutants defective in the production of autophagosomes display significant defects in the degradation of apoptotic cells, demonstrating the importance of autophagosomes to this process. The signaling pathway led by the phagocytic receptor CED-1, the adaptor protein CED-6, and the large GTPase dynamin (DYN-1) promotes the recruitment of autophagosomes to phagosomes. Moreover, the subsequent fusion of autophagosomes with phagosomes requires the functions of the small GTPase RAB-7 and the HOPS complex components. Further observations suggest that autophagosomes provide apoptotic cell-degradation activities in addition to and in parallel of lysosomes. Our findings reveal that, unlike the single-membrane, LC3-associated phagocytosis (LAP) vesicles reported for mammalian phagocytes, the canonical double-membrane autophagosomes facilitate the clearance of C. elegans apoptotic cells. These findings add autophagosomes to the collection of intracellular organelles that contribute to phagosome maturation, identify novel crosstalk between the autophagy and phagosome maturation pathways, and discover the upstream signaling molecules that initiate this crosstalk.

cell biology↗

Detecting the state of drowsiness induced by propofol by spatial filter and machine learning algorithm on EEG recording

To accurately measure the depth of anesthesia has been a challenge for both anesthesiologists and engineers who work on developing tools of measurements. This study aims to use a machine-learning algorithm to predict the drowsy state, a transitional depth of sedation during propofol anesthesia. The data used in this study were scalp EEG (electroencephalogram) recordings selected from the University of Cambridge Repository. Raw EEG recordings were preprocessed into power spectrum matrices one second per sample. A total of 170 samples (110 awake samples and 60 drowsy samples) were used. A CNN (Convolutional Neural Network) for the MNIST (Modified National Institute of Standards and Technology) dataset was applied on these EEG power spectrum matrices. Due to the small dataset volume, Leave-One-Out cross-validation was used to train the data. Results of the training accuracy reached 99.69%. And test accuracy averaged 96.47%. Overall, the model is able to predict the state of drowsiness during propofol anesthesia. This provides the potential to develop EEG monitoring devices with closed-loop feedback of such a machine learning algorithm that controls the titration of the dosage of anesthetic administration and the depth of anesthesia.

neuroscience↗

Native MOWChIP-seq: Genome-wide profiles of key protein bindings reveal functional differences among various brain regions

Genome-wide profiling of interactions between genome and various functional proteins is critical for understanding regulatory processes involved in development and diseases. Conventional assays require a large number of cells and high-quality data on tissue samples are scarce. Here we optimized a low-input chromatin immunoprecipitation followed by sequencing (ChIP-seq) technology for profiling RNA polymerase II (Pol II), transcription factor (TF), and enzyme binding at the genome scale. The new approach, termed native MOWChIP-seq, produces high-quality binding profiles using 1000-50,000 cells. We used the approach to examine the binding of Pol II and two TFs (EGR1 and MEF2C) in cerebellum and prefrontal cortex of mouse brain and found that their binding profiles are highly reflective of the functional differences between the two brain regions. Our analysis reveals the potential for linking genome-wide TF or Pol II profiles with neuroanatomical origins of brain cells.

genomics↗

Mapping the glycosyltransferase fold landscape using deep learning

Glycosyltransferases (GTs) play fundamental roles in nearly all cellular processes through the biosynthesis of complex carbohydrates and glycosylation of diverse protein and small molecule substrates. The extensive structural and functional diversification of GTs presents a major challenge in mapping the relationships connecting sequence, structure, fold and function using traditional bioinformatics approaches. Here, we present a convolutional neural network with attention (CNN-attention) based deep learning model that leverages simple secondary structure representations generated from primary sequences to provide GT fold prediction with high accuracy. The model learned distinguishing features free of primary sequence alignment constraints and, unlike other models, is highly interpretable and helped identify common secondary structural features shared by divergent families. The model delineated sequence and structural features characteristic of individual fold types, while classifying them into distinct clusters that group evolutionarily divergent families based on shared secondary structural features. We further extend our model to classify GT families of unknown folds and variants of known folds. By identifying families that are likely to adopt novel folds such as GT91, GT96 and GT97, our studies identify targets for future structural studies and expand the GT fold landscape.

bioinformatics↗

Polysaccharide utilization loci in Bacteroides determine population fitness and community-level interactions

Polysaccharide utilization loci (PULs) in the human gut microbiome have critical roles in shaping human health and ecological dynamics. We develop a CRISPR-FnCpf1-RecT genome-editing tool to study 23 PULs in the highly abundant species B. uniformis (BU). We identify the glycan-degrading functions of multiple PULs and elucidate transcriptional coordination between PULs that enables the population to adapt to the loss of PULs. Exploiting a pooled BU mutant barcoding strategy, we demonstrate that the in vitro fitness and the colonization ability of BU in the murine gut is enhanced by deletion of specific PULs and modulated by glycan availability. We show that BU PULs can mediate complex glycan-dependent interactions with butyrate producers that depend on the mechanism of degradation and the butyrate producer glycan utilizing ability. In sum, PULs are major determinants of community dynamics and butyrate production and can provide a selective advantage or disadvantage depending on the nutritional landscape.

synthetic biology↗

CBX4 regulates long-form thymic stromal lymphopoietin-mediated airway inflammation through SUMOylation in HDM-induced asthma

RationaleThymic stromal lymphopoietin (TSLP) is present in two distinct isoforms, short-form (sfTSLP) and long-form (lfTSLP). lfTSLP promotes inflammation while sfTSLP inhibits inflammation in allergic asthma. However, little is known about the regulation of lfTSLP and sfTSLP during allergic attack in asthma airway epithelium. Methods and ResultsHere, we report that SUMOylation was enhanced in HDM-induced allergic asthma airway epithelium. Inhibition of SUMOylation significantly alleviated airway Th2 inflammation and lfTSLP expression. Mechanistically, CBX4, a SUMOylation E3 ligase, enhanced lfTSLP, but not sfTSLP, mRNA translation through the RNA binding protein, MEX-3B. MEX-3B promoted lfTSLP translation through binding of its KH domains to the lfTSLP mRNA. Furthermore, CBX4 regulated MEX-3B transcription in HBE through enhancing SUMOylation levels of the transcription factor, TFII-I. ConclusionWe demonstrate an important mechanism whereby CBX4 promotes MEX-3B transcription through enhancing TFII-I SUMOylation, and MEX-3B enhances the expression of lfTSLP through binding to the lfTSLP mRNA and promoting its translation. Our findings uncover a novel target of CBX4 for therapeutic agents to lfTSLP-mediated asthma.

molecular biology↗

Flexibility-aware graph-based algorithm improves antigen epitopes identification

Epitopes of an antigen are the surface residues in the spatial proximity that can be recognized by antibodies. Identifying such residues has shown promising potentiality in vaccine design, drug development and chemotherapy, thus attracting extensive endeavors. Although great efforts have been made, the epitope prediction performance is still unsatisfactory. One possible issue accounting to this poor performance could be the ignorance of structural flexibility of antigens. Flexibility is a natural characteristic of antigens, which has been widely reported. However, this property has never been used by existing models. To this end, we propose a novel flexibility-aware graph-based computational model to identify epitopes. Unlike existing graph-based approaches that take the static structures of antigens as input, we consider all possible variations of the side chains in graph construction. These flexibility-aware graphs, of which the edges are highly enriched, are further partitioned into subgraphs by using a graph clustering algorithm. These clusters are subsequently expanded into larger graphs for detecting overlapping residues between epitopes if exist. Finally, the expanded graphs are classified as epitopes or non-epitopes via a newly designed graph convolutional network. Experimental results show that our flexibility-aware model markedly outperforms existing approaches and promotes the F1-score to 0.656. Comparing to the state-of-the-art, our approach makes an increment of F1-score by 16.3%. Further in-depth analysis demonstrates that the flexibility-aware strategy contributes the most to the improvement. The source codes of the proposed model is freely available at https://github.com/lzhlab/epitope. Author summaryEpitope prediction is helpful to many biomedical applications so that dozens of models have been proposed aiming at improving prediction efficiency and accuracy. However, the performances are still unsatisfactory due to its complicated nature, particularly the noteworthy flexible structures, which makes the precise prediction even more challenging. The existing approaches have overlooked the flexibility during model construction. To this end, we propose a graph model with flexibility heavily involved. Our model is mainly composed of three parts: i) flexibility-aware graph construction; ii) overlapping subgraph clustering; iii) graph convolutional network-based subgraph classification. Experimental results show that our newly proposed model markedly outperforms the existing best ones, making an increment of F1-score by 16.3%.

bioinformatics↗

Single-molecule mechanical unfolding kinetics of unmodified Saccharomyces cerevisiae tRNAPhe: a hint to the tRNA chaperone-tRNA interaction mechanism

The biological activity of tRNA is closely related to its mechanical folding properties. Although previous studies focused on the folding and unfolding mechanism of tRNA, its kinetics are largely unknown. In this study, combining optical tweezers and molecule dynamics simulations, we characterized the mechanical folding and unfolding processes of a single unmodified Saccharomyces cerevisiae tRNAphe. We identified the intermediates and pathways for tRNA mechanical folding and unfolding in the presence of Mg2+, discovering that the folding/unfolding kinetics of D stem-loop and T stem-loop but not the anti-codon stem-loop significantly affected by their upstream and downstream structures. The cooperative unfolding of the tRNA in the presence of Mg2+ lead to a large hysteresis between the folding and unfolding pathway, and such hysteresis and unfolding cooperativity are significantly reduced by lowering the Mg2+ concentration or mutating the nucleotides forming the elbow structure. Moreover, both steered molecular dynamics simulation and optical tweezers experiment results support that, formation of tertiary interactions in the elbow region increases energy barriers of the mechanical unfolding pathway, including those in between intermediates, and determines the overall unfolding cooperativity. Our studies may shed light on the detailed tRNA chaperone mechanism of TruB and TrmA.

biophysics↗

Ultraspecific somatic SNV and indel detection in single neurons using primary template-directed amplification

Primary template-directed amplification (PTA) is an improved amplification technique for single-cell DNA sequencing. We generated whole-genome analysis of 76 single neurons and developed SCAN2, a computational method to accurately identify both clonal and non-clonal somatic (i.e., limited to a single neuron) single nucleotide variants (SNVs) and small insertions and deletions (indels) using PTA data. Our analysis confirms an increase in non-clonal somatic mutation in single neurons with age, but revises estimates for the rate of this accumulation to be 15 SNVs per year. We also identify artifacts in other amplification methods. Most importantly, we show that somatic indels also increase by at least 2 indels per year per neuron and that indels may have a larger impact on gene function than somatic SNVs in human neurons.

genomics↗

Gene co-expression network analysis facilitates identification of novel important genes for the moulting process of the salmon louse (Lepeophtheirus salmonis)

BackgroundThe salmon louse (Lepeophtheirus salmonis) is an obligate ectoparasitic copepod, living on Atlantic salmon and other salmonids in the marine environment. Salmon lice cause a number of environmental problems and lead to large economical losses in aquaculture every year. In order to develop novel parasite control strategies, a better understanding of the mechanisms of moulting and development of the salmon louse at the transcriptional level is required. MethodsThree weighted gene co-expression networks were constructed based on the pairwise correlations of salmon louse gene expression profiles at different life stages. Network-based approaches and gene annotation information were applied to identify genes that might be important for the moulting and development of the salmon louse. RNA interference was performed for validation. Regulatory impact factors were calculated for all the transcription factor genes by examining the changes in co-expression patterns between transcription factor genes and deferentially expressed genes in middle stages and moulting stages. ResultsEight gene modules were predicted as important, and 10 genes from six of the eight modules have been found to show observable phenotypes in RNA interference experiments. We knocked down five hub genes from three modules and observed phenotypic consequences in all experiments. In the infection trial, no copepodids with the RAB1A-like gene knocked down were found on fish, while control samples developed to chalimus-1 larvae. Also, a FOXO-like gene obtained highest scores in the regulatory impact factor calculation. ConclusionsWe propose a gene co-expression network-based approach to identify genes playing an important role in the moulting and development of salmon louse. The RNA interference experiments confirmed the effectiveness of our approach and demonstrated the indispensable role of RAB1A-like gene in the development of salmon louse. In addition to salmon louse, this approach could be generalized to identify important genes associated with a phenotype of interest in other organisms.

bioinformatics↗

Targeting circPTPN12/1 miR-21-5p/ΔNp63α pathway as a therapeutic strategy for human endometrial fibrosis

Emerging evidence demonstrates the important role of circular RNAs (circRNAs) in regulating pathological processes in various diseases including organ fibrosis. Endometrium fibrosis is the leading cause of uterine infertility, but the role of circRNAs in its pathogenesis is largely unknown. Here, we provide the evidence that upregulation of circPTPN12 in endometrial epithelial cells (EECs) of fibrotic endometrium functions as endogenous sponge of miR-21-5p to inhibit miR-21-5p expression and activity, which in turn results in upregulation of {Delta}Np63 to induce the epithelial mesenchymal transition (EMT) of EECs (EEC-EMT). In a mouse model of endometrium fibrosis, circPTPN12 appears to be a cofactor of driving EEC-EMT. Our findings reveal the novel mechanism in the pathogenesis of endometrium fibrosis and the potential therapeutic strategy for endometrium fibrosis via targeting circPTPN12/miR-21-5p/{Delta}Np63 pathway.

molecular biology↗

Towards a comprehensive delineation of white matter tract-related deformation

Finite element (FE) models of the human head are valuable instruments to explore the mechanobiological pathway from external loading, localized brain response, and resultant injury risks. The injury predictability of these models depends on the use of effective criteria as injury predictors. The FE-derived normal deformation along white matter (WM) fiber tracts (i.e., tract-oriented strain) has recently been suggested as an appropriate predictor for axonal injury. However, the tract-oriented strain only represents a partial depiction of the WM fiber tract deformation. A comprehensive delineation of tract-related deformation may improve the injury predictability of the FE head model by delivering new tract-related criteria as injury predictors. Thus, the present study performed a theoretical strain analysis to comprehensively characterize the WM fiber tract deformation by relating the strain tensor of the WM element to its embedded fiber tract. Three new tract-related strains with exact analytical solutions were proposed, measuring the normal deformation perpendicular to the fiber tracts (i.e., tract-perpendicular strain), and shear deformation along and perpendicular to the fiber tracts (i.e., axial-shear strain and lateral-shear strain, respectively). The injury predictability of these three newly-proposed strain peaks along with the previously-used tract-oriented strain peak and maximum principal strain (MPS) were evaluated by simulating 151 impacts with known outcome (concussion or non-concussion). The results preliminarily showed that four tract-related strain peaks exhibited superior performance than MPS in discriminating concussion and non-concussion cases. This study presents a comprehensive quantification of WM tract-related deformation and advocates the use of orientation-dependent strains as criteria for injury prediction, which may ultimately contribute to an advanced mechanobiological understanding and enhanced computational predictability of brain injury.

bioengineering↗

Genome-wide CRISPR activation screen identifies novel receptors for SARS-CoV-2 entry

The ongoing pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been endangering worldwide public health and economy. SARS-CoV-2 infects a variety of tissues where the known receptor ACE2 is low or almost absent, suggesting the existence of alternative pathways for virus entry. Here, we performed a genome-wide barcoded-CRISPRa screen to identify novel host factors that enable SARS-CoV-2 infection. In addition to known host proteins, i.e. ACE2, TMPRSS2 and NRP1, we identified multiple host components, among which LDLRAD3, TMEM30A and CLEC4G were confirmed as functional receptors for SARS-CoV-2. All these membrane proteins bind directly to spikes N-terminal domain (NTD). Their essential and physiological roles have all been confirmed in either neuron or liver cells. In particular, LDLRAD3 and CLEC4G mediate SARS-CoV-2 entry and infection in a fashion independent of ACE2. The identification of the novel receptors and entry mechanisms could advance our understanding of the multiorgan tropism of SARS-CoV-2, and may shed light on the development of the therapeutic countermeasures against COVID-19.

microbiology↗