cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.25729546
title: Genome-wide expanding of genetic evolution and potential pathogenicity in <i>Vibrio alginolyticus</i>

description: <i>Vibrio alginolyticus</i>, an emergent species of <i>Vibrio</i> genus, exists in aquatic and marine environments. It has undergone genetic diversification, but its detailed genomic diversity is still unclear. Here, we performed a multi-dimensional comparative genomic analysis to explore the population phylogeny, virulence-related genes and potential drug resistance genes of 184 <i>V. alginolyticus</i> isolates. Although genetic diversity is complex, we analysed the population structure using three sub-datasets, including the subdivision for three lineages into sublineages and the distribution of strains in the marine ecological niche. Accessory genes, most of which reclassified <i>V. alginolyticus</i> genomes as different but with relatively close affinities, were nonuniformly distributed among these isolates. We demonstrated that the spread of some post-evolutionary isolates (mainly L3 strains isolated from Chinese territorial seas) was likely to be closely related to human activities, whereas other more ancestral strains (strains in the L1 and L2) tended to be locally endemic and formed clonal complex groups. In terms of pathogenicity, the potential virulence factors were mainly associated with toxin, adherence, motility, chemotaxis, and the type III secretion system (T3SS). We also found five types of antibacterial drug resistance genes. The prevalence of β-lactam resistance genes was 100%, which indicated that there may be a potential risk of natural resistance to β-lactam drugs. Our study reveals insights into genomic characteristics, evolution and potential virulence-associated gene profiles of <i>V. alginolyticus</i>.
DOI: 10.6084/m9.figshare.25729546.v2
title: Genome-wide expanding of genetic evolution and potential pathogenicity in <i>Vibrio alginolyticus</i>

description: <i>Vibrio alginolyticus</i>, an emergent species of <i>Vibrio</i> genus, exists in aquatic and marine environments. It has undergone genetic diversification, but its detailed genomic diversity is still unclear. Here, we performed a multi-dimensional comparative genomic analysis to explore the population phylogeny, virulence-related genes and potential drug resistance genes of 184 <i>V. alginolyticus</i> isolates. Although genetic diversity is complex, we analysed the population structure using three sub-datasets, including the subdivision for three lineages into sublineages and the distribution of strains in the marine ecological niche. Accessory genes, most of which reclassified <i>V. alginolyticus</i> genomes as different but with relatively close affinities, were nonuniformly distributed among these isolates. We demonstrated that the spread of some post-evolutionary isolates (mainly L3 strains isolated from Chinese territorial seas) was likely to be closely related to human activities, whereas other more ancestral strains (strains in the L1 and L2) tended to be locally endemic and formed clonal complex groups. In terms of pathogenicity, the potential virulence factors were mainly associated with toxin, adherence, motility, chemotaxis, and the type III secretion system (T3SS). We also found five types of antibacterial drug resistance genes. The prevalence of β-lactam resistance genes was 100%, which indicated that there may be a potential risk of natural resistance to β-lactam drugs. Our study reveals insights into genomic characteristics, evolution and potential virulence-associated gene profiles of <i>V. alginolyticus</i>.
DOI: 10.6084/m9.figshare.25905070
title: <i>In vivo</i> rescue of arboviruses directly from subgenomic DNA fragments

description: Reverse genetic systems are mainly used to rescue recombinant viral strains in cell culture. These tools have also been used to generate, by inoculating infectious clones, viral strains directly in living animals. We previously developed the “Infectious Subgenomic Amplicons” (ISA) method, which enables the rescue of single-stranded positive sense RNA viruses <i>in vitro</i> by transfecting overlapping subgenomic DNA fragments. Here, we provide proof-of-concept for direct <i>in vivo</i> generation of infectious particles following the inoculation of subgenomic amplicons. First, we rescued a strain of tick-borne encephalitis virus in mice to transpose the ISA method <i>in vivo</i>. Subgenomic DNA fragments were amplified using a 3-fragment reverse genetics system and inoculated intramuscularly. Almost all animals were infected when quantities of DNA inoculated were at least 20 µg. We then optimized our procedure in order to increase the animal infection rate. This was achieved by adding an electroporation step and/or using a simplified 2- fragment reverse genetics system. Under optimal conditions, a large majority of animals were infected with doses of 20 ng of DNA. Finally, we demonstrated the versatility of this method by applying it to Japanese encephalitis and Chikungunya viruses. This method provides an efficient strategy for <i>in vivo</i> rescue of arboviruses. Furthermore, in the context of the development of DNA-launched live attenuated vaccines, this new approach may facilitate the generation of attenuated strains <i>in vivo</i>. It also enables to deliver a substance free of any vector DNA, which seems to be an important criterion for the development of human vaccines.
DOI: 10.6084/m9.figshare.25905070.v3
title: <i>In vivo</i> rescue of arboviruses directly from subgenomic DNA fragments

description: Reverse genetic systems are mainly used to rescue recombinant viral strains in cell culture. These tools have also been used to generate, by inoculating infectious clones, viral strains directly in living animals. We previously developed the “Infectious Subgenomic Amplicons” (ISA) method, which enables the rescue of single-stranded positive sense RNA viruses <i>in vitro</i> by transfecting overlapping subgenomic DNA fragments. Here, we provide proof-of-concept for direct <i>in vivo</i> generation of infectious particles following the inoculation of subgenomic amplicons. First, we rescued a strain of tick-borne encephalitis virus in mice to transpose the ISA method <i>in vivo</i>. Subgenomic DNA fragments were amplified using a 3-fragment reverse genetics system and inoculated intramuscularly. Almost all animals were infected when quantities of DNA inoculated were at least 20 µg. We then optimized our procedure in order to increase the animal infection rate. This was achieved by adding an electroporation step and/or using a simplified 2- fragment reverse genetics system. Under optimal conditions, a large majority of animals were infected with doses of 20 ng of DNA. Finally, we demonstrated the versatility of this method by applying it to Japanese encephalitis and Chikungunya viruses. This method provides an efficient strategy for <i>in vivo</i> rescue of arboviruses. Furthermore, in the context of the development of DNA-launched live attenuated vaccines, this new approach may facilitate the generation of attenuated strains <i>in vivo</i>. It also enables to deliver a substance free of any vector DNA, which seems to be an important criterion for the development of human vaccines.
DOI: 10.6084/m9.figshare.25905070.v4
title: <i>In vivo</i> rescue of arboviruses directly from subgenomic DNA fragments

description: Reverse genetic systems are mainly used to rescue recombinant viral strains in cell culture. These tools have also been used to generate, by inoculating infectious clones, viral strains directly in living animals. We previously developed the “Infectious Subgenomic Amplicons” (ISA) method, which enables the rescue of single-stranded positive sense RNA viruses <i>in vitro</i> by transfecting overlapping subgenomic DNA fragments. Here, we provide proof-of-concept for direct <i>in vivo</i> generation of infectious particles following the inoculation of subgenomic amplicons. First, we rescued a strain of tick-borne encephalitis virus in mice to transpose the ISA method <i>in vivo</i>. Subgenomic DNA fragments were amplified using a 3-fragment reverse genetics system and inoculated intramuscularly. Almost all animals were infected when quantities of DNA inoculated were at least 20 µg. We then optimized our procedure in order to increase the animal infection rate. This was achieved by adding an electroporation step and/or using a simplified 2- fragment reverse genetics system. Under optimal conditions, a large majority of animals were infected with doses of 20 ng of DNA. Finally, we demonstrated the versatility of this method by applying it to Japanese encephalitis and Chikungunya viruses. This method provides an efficient strategy for <i>in vivo</i> rescue of arboviruses. Furthermore, in the context of the development of DNA-launched live attenuated vaccines, this new approach may facilitate the generation of attenuated strains <i>in vivo</i>. It also enables to deliver a substance free of any vector DNA, which seems to be an important criterion for the development of human vaccines.
DOI: 10.6084/m9.figshare.26893824.v1
title: The C-terminal amino acid motifs of NS1 protein affect the replication and virulence of naturally NS-truncated H1N1 canine influenza virus

description: The vast majority of data obtained from sequence analysis of influenza A viruses (IAVs) have revealed that nonstructural 1 (NS1) proteins from H1N1 swine, H3N8 equine, H3N2 avian and the correspondent subtypes from dogs have a conserved four C-terminal amino acid motif when independent cross-species transmission occurs between these species. To test the influence of the C-terminal amino acid motifs of NS1 protein on the replication and virulence of IAVs, we systematically generated 7 recombinants, which carried naturally truncated NS1 proteins, and their last four C-terminal residues were replaced with PEQK and SEQK (for H1N1), EPEV and KPEI (for H3N8) and ESEV and ESEI (for H3N2) IAVs. Another recombinant was generated by removing the C-terminal residues by reverse genetics. Remarkably, the ESEI and KPEI motifs circulating in canines largely contributed efficient replication in cultured cells and these had enhanced virulence. In contrast, the avian ESEV motif was only responsible for high pathogenicity in mice. We examined the effects of these motifs upon interferon (IFN) induction. The 7 mutant viruses replicated <i>in vitro</i> in an IFN-independent manner, and the canine SEQK motif was able to induced higher levels of IFN-β in human cell lines. These findings shed further new light on the role of the four C-terminal residues in replication and virulence of IAVs and suggest that these motifs can modulate viral replication in a species-specific manner.
DOI: 10.25549/webster-c100-39695
title: Interviews of city of Los Angeles, Emergency Operations Organization, 1992-08/1992-09

description: Summaries of interviews conducted with personnel from the City of Los Angeles's Emergency Operations Organization, 1992 August - September. PART OF SERIES: In addition to analyzing the 1992 riots as a whole, the Webster Commission also divided into several smaller task forces and study groups, each of which addressed one specific aspect of the civil disturbance. The series consists of reports and appendices produced by five of these groups: the Chronology Team, the Public Officials and Community Team, the LAPD Team, the Comparisons Study Group, and the Inter-Agency Team. Also included are two copies of Webster Scope, a report that interprets the riots and their cumulative effects primarily through graphs, charts, statistics, and figures, and several research memoranda that discuss the legality of several riot-response tactics. PART OF SUBSERIES: Materials related to a final report issued by the Webster Commission's Inter-Agency Team. which evaluated the collaboration between the LAPD and other law enforcement agencies in the advent of the 1992 riots. Included is a copy of the final report and the report's appendices, which are comprised of interviews, memoranda, statistical analyses, handbooks, and other miscellaneous documents.
DOI: 10.6084/m9.figshare.25860604
title: Porin deficiency or plasmid copy number increase mediated carbapenem-resistant <i>Escherichia coli</i> resistance evolution

description: This study investigated resistance evolution mechanisms of conjugated plasmids and bacterial hosts under different concentrations of antibiotic pressure. Ancestral strain ECNX52 was constructed by introducing the <i>bla</i><sub>NDM-5</sub>-carrying IncX3 plasmid into <i>E. coli</i> C600, and was subjected to laboratory evolution under different concentrations of meropenem pressure. Minimal inhibitory concentrations and conjugation frequency were determined. Fitness of these strains was assessed. Whole genome sequencing and transcriptional changes were performed. Ancestral host or plasmids were recombined with evolved hosts or plasmids to verify plasmid or host factors in resistance evolution. Role of the <i>repA</i> mutation on plasmid copy number was determined. Two out of the four clones (EM2N1 and EM2N3) exhibited four-fold increase in MIC when exposed to a continuous pressure of 2 μg/mL MEM (1/32 MIC), by down regulating expression of outer membrane protein <i>ompF</i>. Besides, all four clones displayed four-fold increase in MIC and higher conjugation frequency when subjected to a continuous pressure of 4 μg/mL MEM (1/16 MIC), attributing to increasing plasmid copy number generated by <i>repA</i> D140Y (GAT→TAT) mutation. Bacterial hosts and conjugative plasmids can undergo resistance evolution under certain concentrations of antimicrobial pressure by reducing the expression of outer membrane proteins or increasing plasmid copy numbers.
DOI: 10.6084/m9.figshare.25860604.v1
title: Porin deficiency or plasmid copy number increase mediated carbapenem-resistant <i>Escherichia coli</i> resistance evolution

description: This study investigated resistance evolution mechanisms of conjugated plasmids and bacterial hosts under different concentrations of antibiotic pressure. Ancestral strain ECNX52 was constructed by introducing the <i>bla</i><sub>NDM-5</sub>-carrying IncX3 plasmid into <i>E. coli</i> C600, and was subjected to laboratory evolution under different concentrations of meropenem pressure. Minimal inhibitory concentrations and conjugation frequency were determined. Fitness of these strains was assessed. Whole genome sequencing and transcriptional changes were performed. Ancestral host or plasmids were recombined with evolved hosts or plasmids to verify plasmid or host factors in resistance evolution. Role of the <i>repA</i> mutation on plasmid copy number was determined. Two out of the four clones (EM2N1 and EM2N3) exhibited four-fold increase in MIC when exposed to a continuous pressure of 2 μg/mL MEM (1/32 MIC), by down regulating expression of outer membrane protein <i>ompF</i>. Besides, all four clones displayed four-fold increase in MIC and higher conjugation frequency when subjected to a continuous pressure of 4 μg/mL MEM (1/16 MIC), attributing to increasing plasmid copy number generated by <i>repA</i> D140Y (GAT→TAT) mutation. Bacterial hosts and conjugative plasmids can undergo resistance evolution under certain concentrations of antimicrobial pressure by reducing the expression of outer membrane proteins or increasing plasmid copy numbers.
DOI: 10.6084/m9.figshare.26893824
title: The C-terminal amino acid motifs of NS1 protein affect the replication and virulence of naturally NS-truncated H1N1 canine influenza virus

description: The vast majority of data obtained from sequence analysis of influenza A viruses (IAVs) have revealed that nonstructural 1 (NS1) proteins from H1N1 swine, H3N8 equine, H3N2 avian and the correspondent subtypes from dogs have a conserved four C-terminal amino acid motif when independent cross-species transmission occurs between these species. To test the influence of the C-terminal amino acid motifs of NS1 protein on the replication and virulence of IAVs, we systematically generated 7 recombinants, which carried naturally truncated NS1 proteins, and their last four C-terminal residues were replaced with PEQK and SEQK (for H1N1), EPEV and KPEI (for H3N8) and ESEV and ESEI (for H3N2) IAVs. Another recombinant was generated by removing the C-terminal residues by reverse genetics. Remarkably, the ESEI and KPEI motifs circulating in canines largely contributed efficient replication in cultured cells and these had enhanced virulence. In contrast, the avian ESEV motif was only responsible for high pathogenicity in mice. We examined the effects of these motifs upon interferon (IFN) induction. The 7 mutant viruses replicated <i>in vitro</i> in an IFN-independent manner, and the canine SEQK motif was able to induced higher levels of IFN-β in human cell lines. These findings shed further new light on the role of the four C-terminal residues in replication and virulence of IAVs and suggest that these motifs can modulate viral replication in a species-specific manner.
DOI: 10.6084/m9.figshare.26997252
title: Genomic evolution and rearrangement of CTX-Φ prophage elements in <i>Vibrio cholerae</i> during the 2018–2024 cholera outbreaks in eastern Democratic Republic of the Congo

description: Between 2018 and 2024, we conducted systematic whole-genome sequencing and phylogenomic analysis on 263 <i>V. cholerae</i> O1 isolates from cholera patients across four provinces in the Democratic Republic of Congo (North-Kivu, South-Kivu, Tanganyika, and Kasai Oriental). These isolates were classified into the AFR10d and AFR10e sublineages of AFR10 lineage, originating from the third wave of the seventh El Tor cholera pandemic (7PET). Compared to the strains analysed between 2014 and 2017, both sublineages had few genetic changes in the core genome but recent isolates (2022-2024) had significant CTX prophage rearrangement. AFR10e spread across all four provinces, while AFR10d appeared to be extinct by the end of 2020. Since 2022, most <i>V. cholerae</i> O1 isolates exhibited significant CTX prophage rearrangements, including a tandem repeat of an environmental satellite phage RS1 downstream the <i>ctxB t</i>oxin gene of the CTX-Φ-3 prophage on the large chromosome, as well as two or more arrayed copies of an environmental pre-CTX-Φ prophage precursor on the small chromosome. We used Illumina data for mapping and coverage estimation to identify isolates with unique CTX-Φ genomic features. Gene localization was then determined on MinION-derived assemblies, revealing an organization similar to that of non-O1 <i>V. cholerae</i> isolates found in Asia (O139 VC1374, and environmental O4 VCE232), but never described in <i>V. cholerae</i> O1 El Tor from the third wave. In conclusion, while the core genome of AFR10d and AFR10e showed minimal changes, significant alterations in the CTX-Φ and pre-CTX-Φ prophage content and organization were identified in AFR10e from 2022 onwards.
DOI: 10.6084/m9.figshare.26997252.v2
title: Genomic evolution and rearrangement of CTX-Φ prophage elements in <i>Vibrio cholerae</i> during the 2018–2024 cholera outbreaks in eastern Democratic Republic of the Congo

description: Between 2018 and 2024, we conducted systematic whole-genome sequencing and phylogenomic analysis on 263 <i>V. cholerae</i> O1 isolates from cholera patients across four provinces in the Democratic Republic of Congo (North-Kivu, South-Kivu, Tanganyika, and Kasai Oriental). These isolates were classified into the AFR10d and AFR10e sublineages of AFR10 lineage, originating from the third wave of the seventh El Tor cholera pandemic (7PET). Compared to the strains analysed between 2014 and 2017, both sublineages had few genetic changes in the core genome but recent isolates (2022-2024) had significant CTX prophage rearrangement. AFR10e spread across all four provinces, while AFR10d appeared to be extinct by the end of 2020. Since 2022, most <i>V. cholerae</i> O1 isolates exhibited significant CTX prophage rearrangements, including a tandem repeat of an environmental satellite phage RS1 downstream the <i>ctxB t</i>oxin gene of the CTX-Φ-3 prophage on the large chromosome, as well as two or more arrayed copies of an environmental pre-CTX-Φ prophage precursor on the small chromosome. We used Illumina data for mapping and coverage estimation to identify isolates with unique CTX-Φ genomic features. Gene localization was then determined on MinION-derived assemblies, revealing an organization similar to that of non-O1 <i>V. cholerae</i> isolates found in Asia (O139 VC1374, and environmental O4 VCE232), but never described in <i>V. cholerae</i> O1 El Tor from the third wave. In conclusion, while the core genome of AFR10d and AFR10e showed minimal changes, significant alterations in the CTX-Φ and pre-CTX-Φ prophage content and organization were identified in AFR10e from 2022 onwards.
DOI: 10.6084/m9.figshare.26997252.v1
title: Genomic evolution and rearrangement of CTX-Φ prophage elements in <i>Vibrio cholerae</i> during the 2018-2024 cholera outbreaks in eastern Democratic Republic of the Congo

description: Between 2018 and 2024, we conducted systematic whole-genome sequencing and phylogenomic analysis on 263 <i>V. cholerae</i> O1 isolates from cholera patients across four provinces in the Democratic Republic of Congo (North-Kivu, South-Kivu, Tanganyika, and Kasai Oriental). These isolates were classified into the AFR10d and AFR10e sublineages of AFR10 lineage, originating from the third wave of the seventh El Tor cholera pandemic (7PET). Compared to the strains analysed between 2014 and 2017, both sublineages had few genetic changes in the core genome but recent isolates (2022-2024) had significant CTX prophage rearrangement. AFR10e spread across all four provinces, while AFR10d appeared to be extinct by the end of 2020. Since 2022, most <i>V. cholerae</i> O1 isolates exhibited significant CTX prophage rearrangements, including a tandem repeat of an environmental satellite phage RS1 downstream the <i>ctxB t</i>oxin gene of the CTX-Φ-3 prophage on the large chromosome, as well as two or more arrayed copies of an environmental pre-CTX-Φ prophage precursor on the small chromosome. We used Illumina data for mapping and coverage estimation to identify isolates with unique CTX-Φ genomic features. Gene localisation was then determined on MinION-derived assemblies, revealing an organisation similar to that of non-O1 <i>V. cholerae</i> isolates found in Asia (O139 VC1374, and environmental O4 VCE232), but never described in <i>V. cholerae</i> O1 El Tor from the third wave. In conclusion, while the core genome of AFR10d and AFR10e showed minimal changes, significant alterations the CTX-Φ and pre-CTX-Φ prophage content and organisation were identified in AFR10e from 2022 onwards.