cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7937114
title: Zika virus infection in human placental tissue explants is enhanced in the presence of dengue virus antibodies in-vitro

description: The current Zika virus (ZIKV) outbreak is associated with neurological malformations and disorders in neonates. Areas of increased incidence of malformations may overlap with dengue-hyperendemic areas. ZIKV infection is enhanced by antibodies against dengue virus (DENV) in cell culture and inbred mice. Sufficiently powered clinical studies or primate studies addressing the enhancement of fetal ZIKV infection after previous dengue infection are not available. The human placenta is susceptible to ZIKV in vitro, but it is unknown whether antibody-dependent enhancement of ZIKV infection occurs at the placental barrier. Here we studied ZIKV infection in placental tissue in the presence of DENV-immune sera. Explants from the amniochorionic membrane, the chorionic villi, and the maternal decidua were infected with ZIKV in the presence of DENV type 1-, 2-, or 4-immune sera, or controls. Presence of DENV antibodies of any type enhanced the percentage of successful infections of organ explants between 1.42- and 2.67-fold, and led to a faster replication as well as significantly increased virus production. No enhancement was seen with yellow fever or chikungunya virus control sera. Pre-existing DENV antibodies may pose an increased risk of trans-placental ZIKV transmission.
DOI: 10.6084/m9.figshare.7937114.v1
title: Zika virus infection in human placental tissue explants is enhanced in the presence of dengue virus antibodies in-vitro

description: The current Zika virus (ZIKV) outbreak is associated with neurological malformations and disorders in neonates. Areas of increased incidence of malformations may overlap with dengue-hyperendemic areas. ZIKV infection is enhanced by antibodies against dengue virus (DENV) in cell culture and inbred mice. Sufficiently powered clinical studies or primate studies addressing the enhancement of fetal ZIKV infection after previous dengue infection are not available. The human placenta is susceptible to ZIKV in vitro, but it is unknown whether antibody-dependent enhancement of ZIKV infection occurs at the placental barrier. Here we studied ZIKV infection in placental tissue in the presence of DENV-immune sera. Explants from the amniochorionic membrane, the chorionic villi, and the maternal decidua were infected with ZIKV in the presence of DENV type 1-, 2-, or 4-immune sera, or controls. Presence of DENV antibodies of any type enhanced the percentage of successful infections of organ explants between 1.42- and 2.67-fold, and led to a faster replication as well as significantly increased virus production. No enhancement was seen with yellow fever or chikungunya virus control sera. Pre-existing DENV antibodies may pose an increased risk of trans-placental ZIKV transmission.
DOI: 10.6084/m9.figshare.7937114.v2
title: Zika virus infection in human placental tissue explants is enhanced in the presence of dengue virus antibodies in-vitro

description: The current Zika virus (ZIKV) outbreak is associated with neurological malformations and disorders in neonates. Areas of increased incidence of malformations may overlap with dengue-hyperendemic areas. ZIKV infection is enhanced by antibodies against dengue virus (DENV) in cell culture and inbred mice. Sufficiently powered clinical studies or primate studies addressing the enhancement of fetal ZIKV infection after previous dengue infection are not available. The human placenta is susceptible to ZIKV in vitro, but it is unknown whether antibody-dependent enhancement of ZIKV infection occurs at the placental barrier. Here we studied ZIKV infection in placental tissue in the presence of DENV-immune sera. Explants from the amniochorionic membrane, the chorionic villi, and the maternal decidua were infected with ZIKV in the presence of DENV type 1-, 2-, or 4-immune sera, or controls. Presence of DENV antibodies of any type enhanced the percentage of successful infections of organ explants between 1.42- and 2.67-fold, and led to a faster replication as well as significantly increased virus production. No enhancement was seen with yellow fever or chikungunya virus control sera. Pre-existing DENV antibodies may pose an increased risk of trans-placental ZIKV transmission.
DOI: 10.6084/m9.figshare.7937843
title: Differential transmission of Asian and African Zika virus lineages by <i>Aedes aegypti</i> from New Caledonia

description: Zika virus (ZIKV) is a <i>Flavivirus</i> that is transmitted to humans by <i>Aedes</i> mosquitoes. ZIKV is divided into two phylogenetic lineages, African and Asian. In the Asian lineage, Pacific and American clades have been linked to the recent worldwide outbreak of ZIKV. The aim of this study was to measure the vector competence of <i>Aedes aegypti</i> for seven ZIKV strains belonging to both lineages. We demonstrate that <i>Ae. aegypti</i> from New Caledonia (NC), South Pacific region, is a low-competence vector for Asian ZIKV (&lt;10% transmission efficiency). No significant differences were observed in vector competence with respect to the sampling date and collection site of Asian ZIKV strains used (2014 and 2015 for New Caledonia, Pacific clade, and 2016 for French Guiana, American clade). The ability of the New Caledonian <i>Ae. aegypti</i> to transmit ZIKV is significantly greater for the earlier viral isolates belonging to the African lineage (&gt;37% transmission efficiency after 9 days post-infection) compared to recent ZIKV isolates from African (10% transmission efficiency) and Asian lineages (&lt;10% transmission efficiency). The results of this study demonstrate that <i>Ae. aegypti</i> from NC can become infected and replicate different ZIKV strains belonging to all lineages. Our data emphasize the importance of studying the interaction between vectors and their arboviruses according to each local geographic context. This approach will improve our understanding of arbovirus transmission to prevent their emergence and improve health surveillance.
DOI: 10.6084/m9.figshare.7937843.v1
title: Differential transmission of Asian and African Zika virus lineages by <i>Aedes aegypti</i> from New Caledonia

description: Zika virus (ZIKV) is a <i>Flavivirus</i> that is transmitted to humans by <i>Aedes</i> mosquitoes. ZIKV is divided into two phylogenetic lineages, African and Asian. In the Asian lineage, Pacific and American clades have been linked to the recent worldwide outbreak of ZIKV. The aim of this study was to measure the vector competence of <i>Aedes aegypti</i> for seven ZIKV strains belonging to both lineages. We demonstrate that <i>Ae. aegypti</i> from New Caledonia (NC), South Pacific region, is a low-competence vector for Asian ZIKV (&lt;10% transmission efficiency). No significant differences were observed in vector competence with respect to the sampling date and collection site of Asian ZIKV strains used (2014 and 2015 for New Caledonia, Pacific clade, and 2016 for French Guiana, American clade). The ability of the New Caledonian <i>Ae. aegypti</i> to transmit ZIKV is significantly greater for the earlier viral isolates belonging to the African lineage (&gt;37% transmission efficiency after 9 days post-infection) compared to recent ZIKV isolates from African (10% transmission efficiency) and Asian lineages (&lt;10% transmission efficiency). The results of this study demonstrate that <i>Ae. aegypti</i> from NC can become infected and replicate different ZIKV strains belonging to all lineages. Our data emphasize the importance of studying the interaction between vectors and their arboviruses according to each local geographic context. This approach will improve our understanding of arbovirus transmission to prevent their emergence and improve health surveillance.
DOI: 10.15468/dl.vujr92
title: Occurrence Download

description: A dataset containing 0 species occurrences available in GBIF matching the query:
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 The dataset includes 0 records from 0 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0090010-230530130749713/datasets/export for details.
DOI: 10.25549/pcra-c14-64274
title: Redemption tidings, vol. 44, nos. 1-52, 4 Jan. - 26 Dec. 1968

description: [description english/roman)] Issued weekly.
DOI: 10.6084/m9.figshare.7936883
title: Sensitive detection of <i>Treponema pallidum</i> DNA from the whole blood of patients with syphilis by the nested PCR assay

description: The aim of this work was to investigate the application of the nested PCR assay for the detection of <i>Treponema pallidum</i> (TP) DNA from the blood of patients with different stages of syphilis. In this study, a nested PCR method targeting the <i>Tpp47</i> and <i>polA</i> genes (<i>Tpp47</i>-Tp-PCR and <i>polA</i>-Tp-PCR) was developed to detect TP-DNA in whole blood samples collected from 262 patients with different stages of syphilis (84 primary syphilis, 97 secondary syphilis, and 81 latent syphilis patients). The PCR assay detected <i>T. pallidum</i> DNA in 53.6% and 62.9% of the patients with primary and secondary syphilis, respectively, which was much higher than the detection levels in patients with latent syphilis (7.4%) (both <i>p</i> &lt; 0.001). For primary syphilis, a low RPR (0–16) was correlated with a higher detection rate of TP-DNA, whereas for secondary syphilis, the higher detection rate of blood TP-DNA was correlated with higher blood RPR titers (at or beyond 32). For latent syphilis, TP-DNA was only detectable by PCR in the early phase of the latent infection. Thus, blood RPR titers were correlated with the blood <i>T. pallidum</i> burden, but the correlations varied with primary and secondary syphilis. The results indicate that nested PCR is a sensitive method for detecting blood TP-DNA and is especially useful for detecting early syphilis including primary syphilis and secondary syphilis. The findings also suggest that the PCR assay may be used to complement other methods to enhance the diagnosis of syphilis.
DOI: 10.6084/m9.figshare.7936883.v1
title: Sensitive detection of <i>Treponema pallidum</i> DNA from the whole blood of patients with syphilis by the nested PCR assay

description: The aim of this work was to investigate the application of the nested PCR assay for the detection of <i>Treponema pallidum</i> (TP) DNA from the blood of patients with different stages of syphilis. In this study, a nested PCR method targeting the <i>Tpp47</i> and <i>polA</i> genes (<i>Tpp47</i>-Tp-PCR and <i>polA</i>-Tp-PCR) was developed to detect TP-DNA in whole blood samples collected from 262 patients with different stages of syphilis (84 primary syphilis, 97 secondary syphilis, and 81 latent syphilis patients). The PCR assay detected <i>T. pallidum</i> DNA in 53.6% and 62.9% of the patients with primary and secondary syphilis, respectively, which was much higher than the detection levels in patients with latent syphilis (7.4%) (both <i>p</i> &lt; 0.001). For primary syphilis, a low RPR (0–16) was correlated with a higher detection rate of TP-DNA, whereas for secondary syphilis, the higher detection rate of blood TP-DNA was correlated with higher blood RPR titers (at or beyond 32). For latent syphilis, TP-DNA was only detectable by PCR in the early phase of the latent infection. Thus, blood RPR titers were correlated with the blood <i>T. pallidum</i> burden, but the correlations varied with primary and secondary syphilis. The results indicate that nested PCR is a sensitive method for detecting blood TP-DNA and is especially useful for detecting early syphilis including primary syphilis and secondary syphilis. The findings also suggest that the PCR assay may be used to complement other methods to enhance the diagnosis of syphilis.
DOI: 10.6084/m9.figshare.7937015
title: Rv2346c enhances mycobacterial survival within macrophages by inhibiting TNF-α and IL-6 production via the p38/miRNA/NF-κB pathway

description: The intracellular survival of <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) has a central role in the pathogenesis of tuberculosis. <i>Mtb</i> Rv2346c is a member of 6-kDa early secreted antigenic target family of proteins, which are known to inhibit the host immune responses to promote bacillary persistence in macrophages. However, the mechanism through which Rv2346c participates in <i>Mtb</i> pathogenesis is unclear. In the present study, recombinant Rv2346c protein was synthesized and used to treat Bacillus Calmette–Guérin (BCG)-infected macrophages. The results showed that Rv2346c inhibited the proliferation of BCG-infected macrophages and enhanced the survival of BCG in macrophages. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were upregulated during BCG infection but downregulated by Rv2346c. Additional experiments showed that nuclear transcription factor-κB (NF-κB) in BCG-infected macrophages induced the production of TNF-α and IL-6. In addition, miR-155 and miR-99b had a suppressive effect on NF-κB, and the expression of these miRNAs was promoted by p38. Furthermore, Rv2346c was shown to decrease the activation of NF-κB, whereas it enhanced the phosphorylation of p38 and the expression of miR-155 and miR-99b. The function of Rv2346c was also verified in <i>Mtb</i>-infected mice. The results showed that Rv2346c increased the observed bacterial load and lung injury and downregulated TNF-α and IL-6 in vivo. Overall, our results reveal that Rv2346c enhances mycobacterial survival in macrophages via inhibiting the production of TNF-α and IL-6 in a p38/miRNA/NF-κB pathway-dependent manner, suggesting that Rv2346c acts as a crucial virulence factor in <i>Mtb</i> infection and has potential use as a target for anti-tuberculosis therapy.
DOI: 10.6084/m9.figshare.7937015.v1
title: Rv2346c enhances mycobacterial survival within macrophages by inhibiting TNF-α and IL-6 production via the p38/miRNA/NF-κB pathway

description: The intracellular survival of <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) has a central role in the pathogenesis of tuberculosis. <i>Mtb</i> Rv2346c is a member of 6-kDa early secreted antigenic target family of proteins, which are known to inhibit the host immune responses to promote bacillary persistence in macrophages. However, the mechanism through which Rv2346c participates in <i>Mtb</i> pathogenesis is unclear. In the present study, recombinant Rv2346c protein was synthesized and used to treat Bacillus Calmette–Guérin (BCG)-infected macrophages. The results showed that Rv2346c inhibited the proliferation of BCG-infected macrophages and enhanced the survival of BCG in macrophages. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were upregulated during BCG infection but downregulated by Rv2346c. Additional experiments showed that nuclear transcription factor-κB (NF-κB) in BCG-infected macrophages induced the production of TNF-α and IL-6. In addition, miR-155 and miR-99b had a suppressive effect on NF-κB, and the expression of these miRNAs was promoted by p38. Furthermore, Rv2346c was shown to decrease the activation of NF-κB, whereas it enhanced the phosphorylation of p38 and the expression of miR-155 and miR-99b. The function of Rv2346c was also verified in <i>Mtb</i>-infected mice. The results showed that Rv2346c increased the observed bacterial load and lung injury and downregulated TNF-α and IL-6 in vivo. Overall, our results reveal that Rv2346c enhances mycobacterial survival in macrophages via inhibiting the production of TNF-α and IL-6 in a p38/miRNA/NF-κB pathway-dependent manner, suggesting that Rv2346c acts as a crucial virulence factor in <i>Mtb</i> infection and has potential use as a target for anti-tuberculosis therapy.
DOI: 10.6084/m9.figshare.7937021
title: Overexpression of OqxAB and MacAB efflux pumps contributes to eravacycline resistance and heteroresistance in clinical isolates of <i>Klebsiella pneumoniae</i>

description: This study investigated the characteristics and mechanisms of eravacycline resistance and heteroresistance in clinical <i>Klebsiella pneumoniae</i> isolates. A total of 393 clinical <i>K</i>. <i>pneumoniae</i> isolates were collected and subjected to eravacycline and tigecycline MIC determinations using the agar dilution method. Eravacycline heteroresistance was assessed by a population analysis profile (PAP). The expression levels of efflux pumps and their regulators were determined by quantitative reverse-transcription PCR (qRT-PCR). This study identified 67 eravacycline-nonsusceptible isolates; among the extended-spectrum β-lactamase (ESBL)-positive isolates, eravacycline-nonsusceptible isolates were detected more frequently than tigecycline-nonsusceptible isolates (21.7% vs. 9.4%, <i>p</i> = 0.001). The study sample was observed to include 20 <i>K</i>. <i>pneumoniae</i> isolates with eravacycline heteroresistance. Compared to the reference strain, <i>oqxA</i> or <i>oqxB</i> overexpression was observed in nine eravacycline-nonsusceptible isolates (range, 35.64–309.02-fold) and 13 eravacycline-heteroresistant isolates (8.42–296.34-fold). The overexpression of <i>macA</i> or <i>macB</i> was detected in 12 eravacycline-heteroresistant isolates (3.23–28.35-fold). Overexpression of the efflux pump regulator gene <i>ramA</i> was observed in 11 eravacycline-nonsusceptible isolates (3.33–94.05-fold) and 18 eravacycline-heteroresistant isolates (3.89–571.70-fold). The eravacycline MICs were increased by one–fourfold by overexpression of <i>oqxAB</i> or <i>macAB</i> in three eravacycline-sensitive isolates. In conclusion, the overexpression of OqxAB and MacAB efflux pumps and the transcriptional regulator RamA were suggested to be involved in <i>K</i>. <i>pneumoniae</i> eravacycline resistance and heteroresistance.
DOI: 10.6084/m9.figshare.7937021.v1
title: Overexpression of OqxAB and MacAB efflux pumps contributes to eravacycline resistance and heteroresistance in clinical isolates of <i>Klebsiella pneumoniae</i>

description: This study investigated the characteristics and mechanisms of eravacycline resistance and heteroresistance in clinical <i>Klebsiella pneumoniae</i> isolates. A total of 393 clinical <i>K</i>. <i>pneumoniae</i> isolates were collected and subjected to eravacycline and tigecycline MIC determinations using the agar dilution method. Eravacycline heteroresistance was assessed by a population analysis profile (PAP). The expression levels of efflux pumps and their regulators were determined by quantitative reverse-transcription PCR (qRT-PCR). This study identified 67 eravacycline-nonsusceptible isolates; among the extended-spectrum β-lactamase (ESBL)-positive isolates, eravacycline-nonsusceptible isolates were detected more frequently than tigecycline-nonsusceptible isolates (21.7% vs. 9.4%, <i>p</i> = 0.001). The study sample was observed to include 20 <i>K</i>. <i>pneumoniae</i> isolates with eravacycline heteroresistance. Compared to the reference strain, <i>oqxA</i> or <i>oqxB</i> overexpression was observed in nine eravacycline-nonsusceptible isolates (range, 35.64–309.02-fold) and 13 eravacycline-heteroresistant isolates (8.42–296.34-fold). The overexpression of <i>macA</i> or <i>macB</i> was detected in 12 eravacycline-heteroresistant isolates (3.23–28.35-fold). Overexpression of the efflux pump regulator gene <i>ramA</i> was observed in 11 eravacycline-nonsusceptible isolates (3.33–94.05-fold) and 18 eravacycline-heteroresistant isolates (3.89–571.70-fold). The eravacycline MICs were increased by one–fourfold by overexpression of <i>oqxAB</i> or <i>macAB</i> in three eravacycline-sensitive isolates. In conclusion, the overexpression of OqxAB and MacAB efflux pumps and the transcriptional regulator RamA were suggested to be involved in <i>K</i>. <i>pneumoniae</i> eravacycline resistance and heteroresistance.
DOI: 10.6084/m9.figshare.7937081
title: Enzootic situation and molecular epidemiology of <i>Brucella</i> in livestock from 2011 to 2015 in Qingyang, China

description: A large-scale survey was conducted in domestic animal populations from 2011 to 2015 in Qingyang, China. A total of 448,398 animals from different districts of Qingyang were tested for the presence of <i>Brucella</i>-specific antibodies using the Rose Bengal Plate Test (RBPT) and the Standard Agglutination Test (SAT). From 2011 to 2015, the yearly average positive rates were between 0.04 and 4.75% in the eight counties tested. In addition, the prevalence rates were between 0 and 9.96% in these eight counties. Sheep was the dominant host of <i>Brucella</i> in Qingyang, and the prevalence rate in sheep (2.74%) was higher than those in the other animals tested. Identification of 10 <i>Brucella</i> isolates from sheep confirmed that the epidemic strains were <i>B. melitensis</i> biovar 3 (<i>n</i> = 9) and <i>B. melitensis</i> biovar 1 (<i>n</i> = 1). MLVA-11 (multiple-locus variable-number tandem repeat analysis) analysis of the 10 isolates showed three genotypes: genotype 116 (<i>n</i> = 8), genotype 115 (<i>n</i> = 1) and genotype 136 (<i>n</i> = 1). Furthermore, analysis of the whole-genome sequences of the representative <i>B. melitensis</i> strain QY1 indicated that this isolate was closely related to isolates from China and India. The results of serum epidemiology confirmed that the region of northern Qingyang was a critical <i>Brucella</i> epidemic area and that the disease showed a rising trend, especially from 2013 to 2015. An analysis of the isolate genotypes suggested that sheep brucellosis mainly resulted from conventional <i>B. melitensis</i> (East Mediterranean group), although the external strain (American group) also occurred in Qingyang.
DOI: 10.6084/m9.figshare.7937081.v1
title: Enzootic situation and molecular epidemiology of <i>Brucella</i> in livestock from 2011 to 2015 in Qingyang, China

description: A large-scale survey was conducted in domestic animal populations from 2011 to 2015 in Qingyang, China. A total of 448,398 animals from different districts of Qingyang were tested for the presence of <i>Brucella</i>-specific antibodies using the Rose Bengal Plate Test (RBPT) and the Standard Agglutination Test (SAT). From 2011 to 2015, the yearly average positive rates were between 0.04 and 4.75% in the eight counties tested. In addition, the prevalence rates were between 0 and 9.96% in these eight counties. Sheep was the dominant host of <i>Brucella</i> in Qingyang, and the prevalence rate in sheep (2.74%) was higher than those in the other animals tested. Identification of 10 <i>Brucella</i> isolates from sheep confirmed that the epidemic strains were <i>B. melitensis</i> biovar 3 (<i>n</i> = 9) and <i>B. melitensis</i> biovar 1 (<i>n</i> = 1). MLVA-11 (multiple-locus variable-number tandem repeat analysis) analysis of the 10 isolates showed three genotypes: genotype 116 (<i>n</i> = 8), genotype 115 (<i>n</i> = 1) and genotype 136 (<i>n</i> = 1). Furthermore, analysis of the whole-genome sequences of the representative <i>B. melitensis</i> strain QY1 indicated that this isolate was closely related to isolates from China and India. The results of serum epidemiology confirmed that the region of northern Qingyang was a critical <i>Brucella</i> epidemic area and that the disease showed a rising trend, especially from 2013 to 2015. An analysis of the isolate genotypes suggested that sheep brucellosis mainly resulted from conventional <i>B. melitensis</i> (East Mediterranean group), although the external strain (American group) also occurred in Qingyang.