cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29150123
title: Changes in gene expression levels caused by H3K9me3/H3K9ac modifications are associated with BmCPV infection in <i>Bombyx mori</i>

description: Changes in chromatin accessibility caused by histone modifications regulate gene transcription. However, little is known about associations between gene expression changes caused by histone modifications and viral infections. We investigate the midguts of silkworms infected with <i>Bombyx mori</i> cypovirus (BmCPV) at 48 h and 96 h post infection (CPV48 and CPV96), and corresponding midguts of uninfected silkworms (GUT48 and GUT96) using CUT&Tag-seq and RNA-seq. We report H3K9me3, H3K9ac, and gene expression profiles at the genome-wide level to change with BmCPV infection. Differential H3K9me3 peak-related genes were mainly enriched in MAPK, Wnt, and Hippo signalling pathways; Differential H3K9ac peaks-related genes were mainly enriched in the Hippo signalling, apoptosis, and citrate cycle pathways; and differentially expressed genes (DEGs) were mainly enriched in carbon metabolism, protein processing in endoplasmic reticulum, and glycolysis/gluconeogenesis pathways. Integration analysis between H3K9me3/H3K9ac peaks and gene expression revealed changes in gene expression profiles to be associated with alteration of H3K9me3/H3K9ac at promoters; gene expression correlates negatively with corresponding H3K9me3 signals in gene bodies, and positively with corresponding H3K9ac signals at the transcription start site. Intersection genes with log<sub>2</sub>foldchange of both CUT&Tag-seq peak and RNA-seq FPKM &gt; 1 were screened and annotated. Genes shared by differential H3K9me3 peak-related genes and DEGs were enriched in insect hormone biosynthesis, MAPK signalling, and TGF-beta signalling pathways, and genes shared by differential H3K9ac peak-related genes and DEGs were enriched in glycolysis/gluconeogenesis, TGF-beta signalling, and mitophagy pathways. These results indicate that BmCPV regulates gene expression through H3K9me3/H3K9ac.
DOI: 10.6084/m9.figshare.29150123.v1
title: Changes in gene expression levels caused by H3K9me3/H3K9ac modifications are associated with BmCPV infection in <i>Bombyx mori</i>

description: Changes in chromatin accessibility caused by histone modifications regulate gene transcription. However, little is known about associations between gene expression changes caused by histone modifications and viral infections. We investigate the midguts of silkworms infected with <i>Bombyx mori</i> cypovirus (BmCPV) at 48 h and 96 h post infection (CPV48 and CPV96), and corresponding midguts of uninfected silkworms (GUT48 and GUT96) using CUT&Tag-seq and RNA-seq. We report H3K9me3, H3K9ac, and gene expression profiles at the genome-wide level to change with BmCPV infection. Differential H3K9me3 peak-related genes were mainly enriched in MAPK, Wnt, and Hippo signalling pathways; Differential H3K9ac peaks-related genes were mainly enriched in the Hippo signalling, apoptosis, and citrate cycle pathways; and differentially expressed genes (DEGs) were mainly enriched in carbon metabolism, protein processing in endoplasmic reticulum, and glycolysis/gluconeogenesis pathways. Integration analysis between H3K9me3/H3K9ac peaks and gene expression revealed changes in gene expression profiles to be associated with alteration of H3K9me3/H3K9ac at promoters; gene expression correlates negatively with corresponding H3K9me3 signals in gene bodies, and positively with corresponding H3K9ac signals at the transcription start site. Intersection genes with log<sub>2</sub>foldchange of both CUT&Tag-seq peak and RNA-seq FPKM &gt; 1 were screened and annotated. Genes shared by differential H3K9me3 peak-related genes and DEGs were enriched in insect hormone biosynthesis, MAPK signalling, and TGF-beta signalling pathways, and genes shared by differential H3K9ac peak-related genes and DEGs were enriched in glycolysis/gluconeogenesis, TGF-beta signalling, and mitophagy pathways. These results indicate that BmCPV regulates gene expression through H3K9me3/H3K9ac.
DOI: 10.6084/m9.figshare.29534075.v1
title: Contribution of a LysM domain-containing protein regulated by VicRK to <i>streptococcus sanguinis</i> virulence

description: <i>Streptococcus sanguinis</i> is a commensal member of the oral microbiome involved in opportunistic cardiovascular infections. In the present study, we investigated the contribution of <i>ssa_0094</i>, a gene strongly regulated by the two-component system VicRK, to functions associated with biofilm formation, immune evasion and cardiovascular virulence. <i>In silico</i> analysis showed that <i>ssa_0094</i> encodes a protein with a LysM domain, which is highly conserved among <i>S. sanguinis</i>. Although not an ubiquitous gene, several commensal streptococcal species of the oronasopharynx and zoonotic strains of <i>Streptococcus suis</i> harbour <i>ssa_0094</i> homologues. A <i>ssa_0094</i> isogenic mutant (SK0094) showed defects in initiating biofilms on saliva-coated surfaces, reduced hydrophobicity and lower production of amyloid-like components when compared to the parent strain (SK36) or to the complemented mutant (SK0094+), although it showed mild changes in DNA release and production of H<sub>2</sub>O<sub>2</sub>. Deletion of <i>ssa_0094</i> also impaired <i>S. sanguinis</i> binding to multiple human glycoproteins of plasma and/or extracellular matrix (ECM) (plasminogen, fibronectin, fibrinogen, fibrin, type I collagen and elastin), and promoted clear increases in C3b deposition, and in induction of NEtosis by neutrophils of peripheral blood. Moreover, SK0094 showed impaired invasiveness into HCAEC cells and reduced <i>ex vivo</i> persistence in human blood, but no clear change in virulence in a <i>Galleria mellonella</i> infection model. These findings indicate that <i>ssa_0094</i> is highly conserved within <i>S. sanguinis</i> strains required for biofilm initiation as well as for multiple functions of immune evasion and cardiovascular virulence in <i>S. sanguinis</i> in a host-specific fashion.
DOI: 10.6084/m9.figshare.30465697
title: Newcastle disease virus acquires phosphatidylserine through the budding process to enhance infectivity

description: Newcastle disease, a highly contagious avian illness caused by the Newcastle disease virus (NDV), inflicts substantial economic losses upon the global poultry industry. While NDV is known to enter host cells via multiple pathways, critical aspects of its infection and pathogenic mechanisms, particularly the role of host lipids, remain incompletely understood. Here, we demonstrate that NDV infection strategically manipulates host phosphatidylserine (PS) metabolism to enhance its replication cycle. We found that the NDV hemagglutinin-neuraminidase (HN) protein triggers an elevation in intracellular Ca<sup>2+</sup> levels, which in turn activates the host phospholipid scramblase TMEM16F. This activation leads to the externalization of PS to the outer leaflet of the plasma membrane. Consequently, NDV virions budding from these PS-rich membrane domains acquire a PS-enriched envelope. Mass spectrometry analysis confirmed high PS abundance on the viral surface. These PS-decorated progeny virions then engage host cell PS receptors, specifically the receptor tyrosine kinase TYRO3 and T-cell immunoglobulin and mucin domain-containing receptor 4 (TIM-4), to facilitate enhanced viral adsorption and entry. This process, known as “apoptotic mimicry,” represents a novel, parallel entry pathway for NDV. These findings provide new mechanistic insights into NDV-host interactions and identify the PS scrambling and recognition axis as a potential therapeutic target for developing novel anti-NDV strategies.
DOI: 10.6084/m9.figshare.30465697.v1
title: Newcastle disease virus acquires phosphatidylserine through the budding process to enhance infectivity

description: Newcastle disease, a highly contagious avian illness caused by the Newcastle disease virus (NDV), inflicts substantial economic losses upon the global poultry industry. While NDV is known to enter host cells via multiple pathways, critical aspects of its infection and pathogenic mechanisms, particularly the role of host lipids, remain incompletely understood. Here, we demonstrate that NDV infection strategically manipulates host phosphatidylserine (PS) metabolism to enhance its replication cycle. We found that the NDV hemagglutinin-neuraminidase (HN) protein triggers an elevation in intracellular Ca<sup>2+</sup> levels, which in turn activates the host phospholipid scramblase TMEM16F. This activation leads to the externalization of PS to the outer leaflet of the plasma membrane. Consequently, NDV virions budding from these PS-rich membrane domains acquire a PS-enriched envelope. Mass spectrometry analysis confirmed high PS abundance on the viral surface. These PS-decorated progeny virions then engage host cell PS receptors, specifically the receptor tyrosine kinase TYRO3 and T-cell immunoglobulin and mucin domain-containing receptor 4 (TIM-4), to facilitate enhanced viral adsorption and entry. This process, known as “apoptotic mimicry,” represents a novel, parallel entry pathway for NDV. These findings provide new mechanistic insights into NDV-host interactions and identify the PS scrambling and recognition axis as a potential therapeutic target for developing novel anti-NDV strategies.
DOI: 10.6084/m9.figshare.30582181
title: Rapid detection of Seneca Valley virus based on reverse transcription recombinase polymerase amplification and CRISPR-Cas13a

description: The Seneca Valley virus (SVV) is an emerging novel etiological agent that triggers vesicular stomatitis in pigs. SVV leads to considerable financial detriment to the global swine industry. Availability of expeditious, simple, and precise detection techniques would aid in the diagnosis and control of Seneca Valley disease. In this study, we developed a novel SVV detection assay based on reverse transcription recombinase polymerase amplification (RT-RPA)/CRISPR-Cas13a. This technique can specifically identify SVV with no cross-reactivity with other viruses, such as the porcine reproductive and respiratory syndrome virus, pseudorabies virus, classical swine fever virus, and foot-and-mouth disease virus. It boasts a detection threshold as sensitive as 2.43 copies/μL, matching the proficiency of reverse transcriptase quantitative PCR in clinical diagnostics. The streamlined RT-RPA/CRISPR-Cas13a assay for SVV minimizes procedural complexity and the likelihood of contamination. Integrating this method with nucleic acid acquisition via nucleic acid releaser enables a turnaround time of only 40 min from sample acquisition to result determination, underscoring its suitability for on-site diagnostics and affirming its role as a robust instrument for the monitoring and detection of SVV.
DOI: 10.6084/m9.figshare.30582181.v1
title: Rapid detection of Seneca Valley virus based on reverse transcription recombinase polymerase amplification and CRISPR-Cas13a

description: The Seneca Valley virus (SVV) is an emerging novel etiological agent that triggers vesicular stomatitis in pigs. SVV leads to considerable financial detriment to the global swine industry. Availability of expeditious, simple, and precise detection techniques would aid in the diagnosis and control of Seneca Valley disease. In this study, we developed a novel SVV detection assay based on reverse transcription recombinase polymerase amplification (RT-RPA)/CRISPR-Cas13a. This technique can specifically identify SVV with no cross-reactivity with other viruses, such as the porcine reproductive and respiratory syndrome virus, pseudorabies virus, classical swine fever virus, and foot-and-mouth disease virus. It boasts a detection threshold as sensitive as 2.43 copies/μL, matching the proficiency of reverse transcriptase quantitative PCR in clinical diagnostics. The streamlined RT-RPA/CRISPR-Cas13a assay for SVV minimizes procedural complexity and the likelihood of contamination. Integrating this method with nucleic acid acquisition via nucleic acid releaser enables a turnaround time of only 40 min from sample acquisition to result determination, underscoring its suitability for on-site diagnostics and affirming its role as a robust instrument for the monitoring and detection of SVV.
DOI: 10.6084/m9.figshare.30798029
title: Evolving strategies of intracellular Hypervirulent <i>Klebsiella pneumoniae</i> during phage therapy: Reducing host autophagy and inflammation

description: Hypervirulent <i>Klebsiella pneumoniae</i> (hvKp) presents challenges in infection management due to antibiotic resistance associated with its intracellular persistence. This study investigates the efficacy of phage therapy against intracellular hvKp using a two-stage murine model. We assessed changes in virulence, host survival, and immune responses through phagocytosis assays, transmission electron microscopy, and Western blotting, complemented by transcriptomic and proteomic analyses. Results indicate that phage therapy reduces mortality and modulates bacterial virulence by downregulating capsule production. Following phage exposure, hvKp adapts by enhancing its oxidative stress resistance. Crucially, these adaptations weaken host inflammatory and autophagy responses, enabling better survival within host cells. These adaptations suggest that while phage therapy can mitigate infection severity, the capacity of hvKp to modulate host pathways underscores the complexity of treating intracellular infections and highlights the importance of targeting both bacterial and cellular responses. In this study, we investigated the use of phage therapy against intracellular infections caused by hypervirulent Klebsiella pneumoniae, a bacterium capable of evading antibiotics by residing within host cells. Using a mouse model, we demonstrated that phage therapy improves survival and reduces bacterial virulence. However, exposure to phages prompted the bacterium to enhance its oxidative stress defenses and adapt by suppressing host inflammatory and autophagy responses. These adaptations not only promote bacterial survival within host cells but also result in higher bacterial loads in tissues and organs, potentially leading to chronic infections. This poses a severe threat to immunocompromised individuals, underscoring the dual challenge of phage therapy: while it offers significant therapeutic potential, bacterial adaptations can undermine its efficacy. Our findings provide crucial insights into the host-pathogen dynamics during phage therapy, paving the way for more effective strategies to combat intracellular bacterial infections.
DOI: 10.6084/m9.figshare.30798029.v1
title: Evolving strategies of intracellular Hypervirulent <i>Klebsiella pneumoniae</i> during phage therapy: Reducing host autophagy and inflammation

description: Hypervirulent <i>Klebsiella pneumoniae</i> (hvKp) presents challenges in infection management due to antibiotic resistance associated with its intracellular persistence. This study investigates the efficacy of phage therapy against intracellular hvKp using a two-stage murine model. We assessed changes in virulence, host survival, and immune responses through phagocytosis assays, transmission electron microscopy, and Western blotting, complemented by transcriptomic and proteomic analyses. Results indicate that phage therapy reduces mortality and modulates bacterial virulence by downregulating capsule production. Following phage exposure, hvKp adapts by enhancing its oxidative stress resistance. Crucially, these adaptations weaken host inflammatory and autophagy responses, enabling better survival within host cells. These adaptations suggest that while phage therapy can mitigate infection severity, the capacity of hvKp to modulate host pathways underscores the complexity of treating intracellular infections and highlights the importance of targeting both bacterial and cellular responses. In this study, we investigated the use of phage therapy against intracellular infections caused by hypervirulent Klebsiella pneumoniae, a bacterium capable of evading antibiotics by residing within host cells. Using a mouse model, we demonstrated that phage therapy improves survival and reduces bacterial virulence. However, exposure to phages prompted the bacterium to enhance its oxidative stress defenses and adapt by suppressing host inflammatory and autophagy responses. These adaptations not only promote bacterial survival within host cells but also result in higher bacterial loads in tissues and organs, potentially leading to chronic infections. This poses a severe threat to immunocompromised individuals, underscoring the dual challenge of phage therapy: while it offers significant therapeutic potential, bacterial adaptations can undermine its efficacy. Our findings provide crucial insights into the host-pathogen dynamics during phage therapy, paving the way for more effective strategies to combat intracellular bacterial infections.
DOI: 10.6084/m9.figshare.30294967
title: Antifungal mechanism of ketone volatile organic compounds against <i>Pseudogymnoascus destructans</i>

description: Ketone volatile organic compounds have demonstrated favorable inhibitory activity against a wide range of pathogenic fungi, including <i>Pseudogymnoascus destructans</i> (<i>Pd</i>), the lethal pathogenic fungus responsible for white-nose syndrome in bats. However, the mechanism of fungal inhibition by ketones remains unclear. In this study, we employed transcriptomic analysis to conduct RNA sequencing on <i>Pd</i> treated with 2-undecanone and 2-nonanone, aiming to investigate the effects of these ketones on the gene expression profiles of <i>Pd</i>. The results indicated that 2-undecanone and 2-nonanone inhibit spore germination in <i>Pd</i> and cause significant damage to its mycelium. The minimum inhibitory concentrations (MIC) were determined to be 25.94 μg/mL and 135.41 μg/mL, respectively. Transcriptomic analysis revealed these ketones affects <i>Pd</i> through multiple pathways, inducing lesions in the cell wall and membrane, and disrupting ribosomal stability by interfering with rRNA modifications and ribosome assembly. Additionally, we found that 2-undecanone impacts enzymes involved in the tricarboxylic acid cycle, disrupting energy metabolism by interfering with critical metabolic pathways in aerobic organisms. In contrast, 2-nonanone directly damages <i>Pd</i> DNA, triggering the activation of DNA damage repair mechanisms. This study provides a theoretical basis for exploring novel antifungal strategies targeting <i>Pd</i>, suggesting that ketones may serve as potential in vitro defense and control tools, laying the groundwork for the subsequent development of efficient fumigants.
DOI: 10.6084/m9.figshare.30294967.v1
title: Antifungal mechanism of ketone volatile organic compounds against <i>Pseudogymnoascus destructans</i>

description: Ketone volatile organic compounds have demonstrated favorable inhibitory activity against a wide range of pathogenic fungi, including <i>Pseudogymnoascus destructans</i> (<i>Pd</i>), the lethal pathogenic fungus responsible for white-nose syndrome in bats. However, the mechanism of fungal inhibition by ketones remains unclear. In this study, we employed transcriptomic analysis to conduct RNA sequencing on <i>Pd</i> treated with 2-undecanone and 2-nonanone, aiming to investigate the effects of these ketones on the gene expression profiles of <i>Pd</i>. The results indicated that 2-undecanone and 2-nonanone inhibit spore germination in <i>Pd</i> and cause significant damage to its mycelium. The minimum inhibitory concentrations (MIC) were determined to be 25.94 μg/mL and 135.41 μg/mL, respectively. Transcriptomic analysis revealed these ketones affects <i>Pd</i> through multiple pathways, inducing lesions in the cell wall and membrane, and disrupting ribosomal stability by interfering with rRNA modifications and ribosome assembly. Additionally, we found that 2-undecanone impacts enzymes involved in the tricarboxylic acid cycle, disrupting energy metabolism by interfering with critical metabolic pathways in aerobic organisms. In contrast, 2-nonanone directly damages <i>Pd</i> DNA, triggering the activation of DNA damage repair mechanisms. This study provides a theoretical basis for exploring novel antifungal strategies targeting <i>Pd</i>, suggesting that ketones may serve as potential in vitro defense and control tools, laying the groundwork for the subsequent development of efficient fumigants.
DOI: 10.6084/m9.figshare.28550722
title: The role of glutathione for oxidative stress and pathogenicity of <i>Streptococcus suis</i>

description: <i>Streptococcus suis</i> is an important zoonotic pathogen that threatens human and pig health. During infection, the host can impose oxidative stress to resist pathogen invasion. Resistance to oxidative toxicity is an important factor for pathogens. Glutathione synthesis contributes to reactive oxygen species (ROS) detoxification in bacterial cells. Little is known about the roles of glutathione synthesis and transport in <i>S</i>. <i>suis</i>. In this study, we demonstrated that glutathione treatment increased oxidative stress tolerance in <i>S</i>. <i>suis</i>. GshAB and GshT were found in <i>S</i>. <i>suis</i> glutathione synthesis and import by bioinformatics. In vitro, inactivation of <i>gshAB</i> and <i>gshT</i> led to increased sensitivity to oxidative stress. Inactivation of <i>gshT</i> led to growth defects in the medium. The intracellular glutathione content of <i>gshAB</i> or <i>gshT</i> deletion mutants was lower than that of wild type (WT) strain. The phagocytic resistance of <i>gshAB</i> and <i>gshT</i> mutants was lower than that of the WT strain. Moreover, the virulence of <i>gshAB</i> and <i>gshT</i> deletion mutants was significantly lower than that of the WT strain in mouse survival and tissue loading experiments. In conclusion, these results revealed the functions of GshAB and GshT in the pathogenesis of <i>S. suis</i>. These findings enhance our understanding of bacterial virulence mechanisms and may provide a new avenue for therapeutic intervention aimed at curbing <i>S. suis</i> infections.
DOI: 10.6084/m9.figshare.28550722.v1
title: The role of glutathione for oxidative stress and pathogenicity of <i>Streptococcus suis</i>

description: <i>Streptococcus suis</i> is an important zoonotic pathogen that threatens human and pig health. During infection, the host can impose oxidative stress to resist pathogen invasion. Resistance to oxidative toxicity is an important factor for pathogens. Glutathione synthesis contributes to reactive oxygen species (ROS) detoxification in bacterial cells. Little is known about the roles of glutathione synthesis and transport in <i>S</i>. <i>suis</i>. In this study, we demonstrated that glutathione treatment increased oxidative stress tolerance in <i>S</i>. <i>suis</i>. GshAB and GshT were found in <i>S</i>. <i>suis</i> glutathione synthesis and import by bioinformatics. In vitro, inactivation of <i>gshAB</i> and <i>gshT</i> led to increased sensitivity to oxidative stress. Inactivation of <i>gshT</i> led to growth defects in the medium. The intracellular glutathione content of <i>gshAB</i> or <i>gshT</i> deletion mutants was lower than that of wild type (WT) strain. The phagocytic resistance of <i>gshAB</i> and <i>gshT</i> mutants was lower than that of the WT strain. Moreover, the virulence of <i>gshAB</i> and <i>gshT</i> deletion mutants was significantly lower than that of the WT strain in mouse survival and tissue loading experiments. In conclusion, these results revealed the functions of GshAB and GshT in the pathogenesis of <i>S. suis</i>. These findings enhance our understanding of bacterial virulence mechanisms and may provide a new avenue for therapeutic intervention aimed at curbing <i>S. suis</i> infections.