cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7937048.v2
title: Replication and pathogenic potential of influenza A virus subtypes H3, H7, and H15 from free-range ducks in Bangladesh in mammals

description: Surveillance of wild aquatic birds and free-range domestic ducks in the Tanguar Haor wetlands in Bangladesh has identified influenza virus subtypes H3N6, H7N1, H7N5, H7N9, and H15N9. Molecular characterization of these viruses indicates their contribution to the genesis of new genotypes of H5N1 influenza viruses from clade 2.3.2.1a that are dominant in poultry markets in Bangladesh as well as to the genesis of the highly pathogenic H5N8 virus currently causing disease outbreaks in domestic poultry in Europe and the Middle East. Therefore, we studied the antigenicity, replication, and pathogenicity of influenza viruses isolated from Tanguar Haor in the DBA/2J mouse model. All viruses replicated in the lung without prior mammalian adaptation, and H7N1 and H7N9 viruses caused 100% and 60% mortality, respectively. H7N5 viruses replicated only in the lungs, whereas H7N1 and H7N9 viruses also replicated in the heart, liver, and brain. Replication and transmission studies in mallard ducks showed that H7N1 and H7N9 viruses replicated in ducks without clinical signs of disease and shed at high titers from the cloaca of infected and contact ducks, which could facilitate virus transmission and spread. Our results indicate that H7 avian influenza viruses from free-range ducks can replicate in mammals, cause severe disease, and be efficiently transmitted to contact ducks. Our study highlights the role of free-range ducks in the spread of influenza viruses to other species in live poultry markets and the potential for these viruses to infect and cause disease in mammals.
DOI: 10.6084/m9.figshare.7937102
title: Genomic characterization and infectivity of a novel SARS-like coronavirus in Chinese bats

description: SARS coronavirus (SARS-CoV), the causative agent of the large SARS outbreak in 2003, originated in bats. Many SARS-like coronaviruses (SL-CoVs) have been detected in bats, particularly those that reside in China, Europe, and Africa. To further understand the evolutionary relationship between SARS-CoV and its reservoirs, 334 bats were collected from Zhoushan city, Zhejiang province, China, between 2015 and 2017. PCR amplification of the conserved coronaviral protein RdRp detected coronaviruses in 26.65% of bats belonging to this region, and this number was influenced by seasonal changes. Full genomic analyses of the two new SL-CoVs from Zhoushan (ZXC21 and ZC45) showed that their genomes were 29,732 nucleotides (nt) and 29,802 nt in length, respectively, with 13 open reading frames (ORFs). These results revealed 81% shared nucleotide identity with human/civet SARS CoVs, which was more distant than that observed previously for bat SL-CoVs in China. Importantly, using pathogenic tests, we found that the virus can reproduce and cause disease in suckling rats, and further studies showed that the virus-like particles can be observed in the brains of suckling rats by electron microscopy. Thus, this study increased our understanding of the genetic diversity of the SL-CoVs carried by bats and also provided a new perspective to study the possibility of cross-species transmission of SL-CoVs using suckling rats as an animal model.
DOI: 10.6084/m9.figshare.7937102.v1
title: Genomic characterization and infectivity of a novel SARS-like coronavirus in Chinese bats

description: SARS coronavirus (SARS-CoV), the causative agent of the large SARS outbreak in 2003, originated in bats. Many SARS-like coronaviruses (SL-CoVs) have been detected in bats, particularly those that reside in China, Europe, and Africa. To further understand the evolutionary relationship between SARS-CoV and its reservoirs, 334 bats were collected from Zhoushan city, Zhejiang province, China, between 2015 and 2017. PCR amplification of the conserved coronaviral protein RdRp detected coronaviruses in 26.65% of bats belonging to this region, and this number was influenced by seasonal changes. Full genomic analyses of the two new SL-CoVs from Zhoushan (ZXC21 and ZC45) showed that their genomes were 29,732 nucleotides (nt) and 29,802 nt in length, respectively, with 13 open reading frames (ORFs). These results revealed 81% shared nucleotide identity with human/civet SARS CoVs, which was more distant than that observed previously for bat SL-CoVs in China. Importantly, using pathogenic tests, we found that the virus can reproduce and cause disease in suckling rats, and further studies showed that the virus-like particles can be observed in the brains of suckling rats by electron microscopy. Thus, this study increased our understanding of the genetic diversity of the SL-CoVs carried by bats and also provided a new perspective to study the possibility of cross-species transmission of SL-CoVs using suckling rats as an animal model.
DOI: 10.6084/m9.figshare.7936835
title: Molecular determinants of Yellow Fever Virus pathogenicity in Syrian Golden Hamsters: one mutation away from virulence

description: Yellow fever virus <i>(Flavivirus</i> genus) is an arthropod-borne pathogen, which can infect humans, causing a severe viscerotropic disease with a high mortality rate. Adapted viral strains allow the reproduction of yellow fever disease in hamsters with features similar to the human disease. Here, we used the Infectious Subgenomic Amplicons reverse genetics method to produce an equivalent to the hamster-virulent strain, Yellow Fever <i>Ap7</i>, by introducing a set of four synonymous and six nonsynonymous mutations into a single subgenomic amplicon, derived from the sequence of the <i>Asibi</i> strain. The resulting strain, Yellow Fever <i>Ap7M</i>, induced a disease similar to that described for <i>Ap7</i> in terms of symptoms, weight evolution, viral loads in the liver and lethality. Using the same methodology, we produced mutant strains derived from either <i>Ap7M</i> or <i>Asibi</i> viruses and investigated the role of each of <i>Ap7M</i> nonsynonymous mutations in its in vivo phenotype. This allowed identifying key components of the virulence mechanism in hamsters. In <i>Ap7M</i> virus, the reversion of either E/Q27H or E/D155A mutations led to an important reduction of both virulence and in vivo replicative fitness. In addition, the introduction of the single D155A <i>Ap7M</i> mutation within the E protein of the <i>Asibi</i> virus was sufficient to drastically modify its phenotype in hamsters toward both a greater replication efficiency and virulence. Finally, inspection of the <i>Asibi</i> strain E protein structure combined to in vivo testing revealed the importance of an exposed α-helix in domain I, containing residues 154 and 155, for <i>Ap7M</i> virulence in hamsters.
DOI: 10.6084/m9.figshare.7936835.v1
title: Molecular determinants of Yellow Fever Virus pathogenicity in Syrian Golden Hamsters: one mutation away from virulence

description: Yellow fever virus <i>(Flavivirus</i> genus) is an arthropod-borne pathogen, which can infect humans, causing a severe viscerotropic disease with a high mortality rate. Adapted viral strains allow the reproduction of yellow fever disease in hamsters with features similar to the human disease. Here, we used the Infectious Subgenomic Amplicons reverse genetics method to produce an equivalent to the hamster-virulent strain, Yellow Fever <i>Ap7</i>, by introducing a set of four synonymous and six nonsynonymous mutations into a single subgenomic amplicon, derived from the sequence of the <i>Asibi</i> strain. The resulting strain, Yellow Fever <i>Ap7M</i>, induced a disease similar to that described for <i>Ap7</i> in terms of symptoms, weight evolution, viral loads in the liver and lethality. Using the same methodology, we produced mutant strains derived from either <i>Ap7M</i> or <i>Asibi</i> viruses and investigated the role of each of <i>Ap7M</i> nonsynonymous mutations in its in vivo phenotype. This allowed identifying key components of the virulence mechanism in hamsters. In <i>Ap7M</i> virus, the reversion of either E/Q27H or E/D155A mutations led to an important reduction of both virulence and in vivo replicative fitness. In addition, the introduction of the single D155A <i>Ap7M</i> mutation within the E protein of the <i>Asibi</i> virus was sufficient to drastically modify its phenotype in hamsters toward both a greater replication efficiency and virulence. Finally, inspection of the <i>Asibi</i> strain E protein structure combined to in vivo testing revealed the importance of an exposed α-helix in domain I, containing residues 154 and 155, for <i>Ap7M</i> virulence in hamsters.
DOI: 10.6084/m9.figshare.7936844
title: The emergence and spread of one Coxsackievirus A16 Genogroup D novel recombinant strain that caused a clustering HFMD outbreak in Shanghai, China, 2016

description: The emergence and spread of one Coxsackievirus A16 Genogroup D novel recombinant strain that caused a clustering HFMD outbreak in Shanghai, China, 2016
DOI: 10.6084/m9.figshare.7936844.v1
title: The emergence and spread of one Coxsackievirus A16 Genogroup D novel recombinant strain that caused a clustering HFMD outbreak in Shanghai, China, 2016

description: The emergence and spread of one Coxsackievirus A16 Genogroup D novel recombinant strain that caused a clustering HFMD outbreak in Shanghai, China, 2016
DOI: 10.6084/m9.figshare.7937048.v1
title: Replication and pathogenic potential of influenza A virus subtypes H3, H7, and H15 from free-range ducks in Bangladesh in mammals

description: Surveillance of wild aquatic birds and free-range domestic ducks in the Tanguar Haor wetlands in Bangladesh has identified influenza virus subtypes H3N6, H7N1, H7N5, H7N9, and H15N9. Molecular characterization of these viruses indicates their contribution to the genesis of new genotypes of H5N1 influenza viruses from clade 2.3.2.1a that are dominant in poultry markets in Bangladesh as well as to the genesis of the highly pathogenic H5N8 virus currently causing disease outbreaks in domestic poultry in Europe and the Middle East. Therefore, we studied the antigenicity, replication, and pathogenicity of influenza viruses isolated from Tanguar Haor in the DBA/2J mouse model. All viruses replicated in the lung without prior mammalian adaptation, and H7N1 and H7N9 viruses caused 100% and 60% mortality, respectively. H7N5 viruses replicated only in the lungs, whereas H7N1 and H7N9 viruses also replicated in the heart, liver, and brain. Replication and transmission studies in mallard ducks showed that H7N1 and H7N9 viruses replicated in ducks without clinical signs of disease and shed at high titers from the cloaca of infected and contact ducks, which could facilitate virus transmission and spread. Our results indicate that H7 avian influenza viruses from free-range ducks can replicate in mammals, cause severe disease, and be efficiently transmitted to contact ducks. Our study highlights the role of free-range ducks in the spread of influenza viruses to other species in live poultry markets and the potential for these viruses to infect and cause disease in mammals.
DOI: 10.15468/dl.vfgpbb
title: Occurrence Download

description: A dataset containing 4967 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Geometry POLYGON ((-86.8151847999999973 33.4487827000000024, -86.8151847999999973 33.4506747499999975, -86.8151847999999973 33.4530119900000003, -86.8151847999999973 33.4555718200000030, -86.8151847999999973 33.4574638699999980, -86.8151847999999973 33.4599124000000003, -86.8139604899999995 33.4599124000000003, -86.8116231500000026 33.4599124000000003, -86.8086180100000036 33.4599124000000003, -86.8067258899999956 33.4599124000000003, -86.8050563599999947 33.4599124000000003, -86.8030529300000069 33.4599124000000003, -86.8002704000000023 33.4599124000000003, -86.8002704000000023 33.4582429499999989, -86.8002704000000023 33.4552379300000027, -86.8002704000000023 33.4531232799999998, -86.8002704000000023 33.4508973399999974, -86.8002704000000023 33.4487827000000024, -86.8016060100000004 33.4487827000000024, -86.8039433499999973 33.4487827000000024, -86.8069484899999964 33.4487827000000024, -86.8089519199999984 33.4487827000000024, -86.8115118500000023 33.4487827000000024, -86.8135152800000043 33.4487827000000024, -86.8151847999999973 33.4487827000000024))",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "Year is greater than or equal to 1932",
 "BasisOfRecord is one of (Human Observation, Living Specimen, Observation, Specimen, Machine Observation)"
 ]
}

 The dataset includes 4967 records from 7 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0073437-220831081235567/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.25549/pcra-c14-66104
title: Redemption tidings, vol. 46, nos. 1-53, 1 Jan. - 31 Dec. 1970

description: [description english/roman)] Issued weekly.
DOI: 10.6084/m9.figshare.7936856
title: Complete genome analysis demonstrates multiple introductions of enterovirus 71 and coxsackievirus A16 recombinant strains into Thailand during the past decade

description: Hand, foot, and mouth disease (HFMD) caused by enteroviruses remains a public health threat, particularly in the Asia-Pacific region during the past two decades. Moreover, the introduction of multiple subgenotypes and the emergence of recombinant viruses is of epidemiological importance. Based on either the full genome or VP1 sequences, 32 enteroviruses (30 from HFMD patients, 1 from an encephalitic patient, and 1 from an asymptomatic contact case) isolated in Thailand between 2006 and 2014 were identified as 25 enterovirus 71 (EV71) isolates (comprising 20 B5, 1 C2, 2 C4a, and 2 C4b subgenotypes) and 7 coxsackievirus A16 (CA16) isolates (comprising 6 B1a and 1 B1b subgenotypes). The EV71 subgenotype C4b was introduced into Thailand for the first time in 2006 and was replaced by subgenotype C4a strains in 2009. Phylogenetic, similarity plot and bootscan analyses of the complete viral genomes identified 12 recombinant viruses among the 32 viral isolates. Only one EV71-B5 isolate out of 20 was a recombinant virus with one region of intratypic or intertypic recombination, while all four EV71-C4 isolates were recombinant viruses having undergone double recombination, and all seven CA16 isolates were recombinant viruses. The recombination breakpoints of these recombinants are located solely within the P2 and P3 regions. Surveillance for circulating strains and subgenotype replacement are important with respect to molecular epidemiology and the selection of the upcoming EV71 vaccine. In addition, the clinical importance of recombinant viruses needs to be further explored.
DOI: 10.6084/m9.figshare.7936856.v1
title: Complete genome analysis demonstrates multiple introductions of enterovirus 71 and coxsackievirus A16 recombinant strains into Thailand during the past decade

description: Hand, foot, and mouth disease (HFMD) caused by enteroviruses remains a public health threat, particularly in the Asia-Pacific region during the past two decades. Moreover, the introduction of multiple subgenotypes and the emergence of recombinant viruses is of epidemiological importance. Based on either the full genome or VP1 sequences, 32 enteroviruses (30 from HFMD patients, 1 from an encephalitic patient, and 1 from an asymptomatic contact case) isolated in Thailand between 2006 and 2014 were identified as 25 enterovirus 71 (EV71) isolates (comprising 20 B5, 1 C2, 2 C4a, and 2 C4b subgenotypes) and 7 coxsackievirus A16 (CA16) isolates (comprising 6 B1a and 1 B1b subgenotypes). The EV71 subgenotype C4b was introduced into Thailand for the first time in 2006 and was replaced by subgenotype C4a strains in 2009. Phylogenetic, similarity plot and bootscan analyses of the complete viral genomes identified 12 recombinant viruses among the 32 viral isolates. Only one EV71-B5 isolate out of 20 was a recombinant virus with one region of intratypic or intertypic recombination, while all four EV71-C4 isolates were recombinant viruses having undergone double recombination, and all seven CA16 isolates were recombinant viruses. The recombination breakpoints of these recombinants are located solely within the P2 and P3 regions. Surveillance for circulating strains and subgenotype replacement are important with respect to molecular epidemiology and the selection of the upcoming EV71 vaccine. In addition, the clinical importance of recombinant viruses needs to be further explored.
DOI: 10.6084/m9.figshare.7936814
title: Characterising routes of H5N1 and H7N9 spread in China using Bayesian phylogeographical analysis

description: Avian influenza H5N1 subtype has caused a global public health concern due to its high pathogenicity in poultry and high case fatality rates in humans. The recently emerged H7N9 is a growing pandemic risk due to its sustained high rates of human infections, and recently acquired high pathogenicity in poultry. Here, we used Bayesian phylogeography on 265 H5N1 and 371 H7N9 haemagglutinin sequences isolated from humans, animals and the environment, to identify and compare migration patterns and factors predictive of H5N1 and H7N9 diffusion rates in China. H7N9 diffusion dynamics and predictor contributions differ from H5N1. Key determinants of spatial diffusion included: proximity between locations (for H5N1 and H7N9), and lower rural population densities (H5N1 only). For H7N9, additional predictors included low avian influenza vaccination rates, low percentage of nature reserves and high humidity levels. For both H5N1 and H7N9, we found viral migration rates from Guangdong to Guangxi and Guangdong to Hunan were highly supported transmission routes (Bayes Factor &gt; 30). We show fundamental differences in wide-scale transmission dynamics between H5N1 and H7N9. Importantly, this indicates that avian influenza initiatives designed to control H5N1 may not be sufficient for controlling the H7N9 epidemic. We suggest control and prevention activities to specifically target poultry transportation networks between Central, Pan-Pearl River Delta and South-West regions.
DOI: 10.6084/m9.figshare.7936814.v2
title: Characterising routes of H5N1 and H7N9 spread in China using Bayesian phylogeographical analysis

description: Avian influenza H5N1 subtype has caused a global public health concern due to its high pathogenicity in poultry and high case fatality rates in humans. The recently emerged H7N9 is a growing pandemic risk due to its sustained high rates of human infections, and recently acquired high pathogenicity in poultry. Here, we used Bayesian phylogeography on 265 H5N1 and 371 H7N9 haemagglutinin sequences isolated from humans, animals and the environment, to identify and compare migration patterns and factors predictive of H5N1 and H7N9 diffusion rates in China. H7N9 diffusion dynamics and predictor contributions differ from H5N1. Key determinants of spatial diffusion included: proximity between locations (for H5N1 and H7N9), and lower rural population densities (H5N1 only). For H7N9, additional predictors included low avian influenza vaccination rates, low percentage of nature reserves and high humidity levels. For both H5N1 and H7N9, we found viral migration rates from Guangdong to Guangxi and Guangdong to Hunan were highly supported transmission routes (Bayes Factor &gt; 30). We show fundamental differences in wide-scale transmission dynamics between H5N1 and H7N9. Importantly, this indicates that avian influenza initiatives designed to control H5N1 may not be sufficient for controlling the H7N9 epidemic. We suggest control and prevention activities to specifically target poultry transportation networks between Central, Pan-Pearl River Delta and South-West regions.
DOI: 10.6084/m9.figshare.7937123
title: miR-1303 regulates BBB permeability and promotes CNS lesions following CA16 infections by directly targeting MMP9

description: Coxsackievirus A16 (CA16) is a member of the Picornaviridae family and causes mild and self-limiting hand, foot, and mouth disease (HFMD) in infants and young children. CA16 infection can also progress to central nervous system (CNS) complications; however, the underlying mechanism by which CA16 penetrates the blood-brain barrier (BBB) and then causes CNS damage remains unclear. This study aimed to explore the mechanism of CA16 neurotropic tropism by establishing an in vitro BBB model with CA16 infection and an in vivo CA16 rhesus monkey infant infection model. The results showed that CA16 infection induced increased permeability of the BBB accompanied by upregulation of matrix metalloproteinase 9 (MMP9) expression. Subsequently, high-throughput miRNA sequencing technology and bioinformatics analysis revealed that miR-1303 may regulate BBB permeability by targeting MMP9. Next, we used dual-luciferase, qRT-PCR, and western blot assays to provide evidence of MMP9 targeting by miR-1303. Further experiments revealed that CA16 infection promoted the degradation of junctional complexes (Claudin4, Claudin5, VE-Cadherin, and ZO-1), likely by downregulating miR-1303 and upregulating MMP9. Finally, EGFP-CA16 infection could enter the CNS by facilitating the degradation of junctional complexes, eventually causing neuroinflammation and injury to the CNS, which was confirmed using the in vivo rhesus monkey model. Our results indicate that CA16 might penetrate the BBB and then enter the CNS by downregulating miR-1303, which disrupts junctional complexes by directly regulating MMP9 and ultimately causing pathological CNS changes. These results provide new therapeutic targets in HFMD patients following CA16 infection.
DOI: 10.6084/m9.figshare.7937123.v1
title: miR-1303 regulates BBB permeability and promotes CNS lesions following CA16 infections by directly targeting MMP9

description: Coxsackievirus A16 (CA16) is a member of the Picornaviridae family and causes mild and self-limiting hand, foot, and mouth disease (HFMD) in infants and young children. CA16 infection can also progress to central nervous system (CNS) complications; however, the underlying mechanism by which CA16 penetrates the blood-brain barrier (BBB) and then causes CNS damage remains unclear. This study aimed to explore the mechanism of CA16 neurotropic tropism by establishing an in vitro BBB model with CA16 infection and an in vivo CA16 rhesus monkey infant infection model. The results showed that CA16 infection induced increased permeability of the BBB accompanied by upregulation of matrix metalloproteinase 9 (MMP9) expression. Subsequently, high-throughput miRNA sequencing technology and bioinformatics analysis revealed that miR-1303 may regulate BBB permeability by targeting MMP9. Next, we used dual-luciferase, qRT-PCR, and western blot assays to provide evidence of MMP9 targeting by miR-1303. Further experiments revealed that CA16 infection promoted the degradation of junctional complexes (Claudin4, Claudin5, VE-Cadherin, and ZO-1), likely by downregulating miR-1303 and upregulating MMP9. Finally, EGFP-CA16 infection could enter the CNS by facilitating the degradation of junctional complexes, eventually causing neuroinflammation and injury to the CNS, which was confirmed using the in vivo rhesus monkey model. Our results indicate that CA16 might penetrate the BBB and then enter the CNS by downregulating miR-1303, which disrupts junctional complexes by directly regulating MMP9 and ultimately causing pathological CNS changes. These results provide new therapeutic targets in HFMD patients following CA16 infection.
DOI: 10.15468/dl.achfvu
title: Occurrence Download

description: A dataset containing 203 species occurrences available in GBIF matching the query:
{
 "and" : [
 "BasisOfRecord is Specimen",
 "HasCoordinate is true",
 "TaxonKey is Adenanthos macropodianus E.C.Nelson",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 203 records from 4 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0054754-200221144449610/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.