Feces metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB13596 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR384565_1.fastq.gz | Fastqsanger.gz | |||
| DRR384566_1.fastq.gz | Fastqsanger.gz | |||
| DRR384567_1.fastq.gz | Fastqsanger.gz | |||
| DRR384568_1.fastq.gz | Fastqsanger.gz | |||
| DRR384569_1.fastq.gz | Fastqsanger.gz |
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Project description:Sanhong Liu, Shigui Ruan & Xinan Zhang. Nonlinear dynamics of avian influenza epidemic models. Mathematical Biosciences 283 (2017).
Avian influenza is a zoonotic disease caused by the transmission of the avian influenza A virus, such as H5N1 and H7N9, from birds to humans. The avian influenza A H5N1 virus has caused more than 500 human infections worldwide with nearly a 60% death rate since it was first reported in Hong Kong in 1997. The four outbreaks of the avian influenza A H7N9 in China from March 2013 to June 2016 have resulted in 580 human cases including 202 deaths with a death rate of nearly 35%. In this paper, we construct two avian influenza bird-to-human transmission models with different growth laws of the avian population, one with logistic growth and the other with Allee effect, and analyze their dynamical behavior. We obtain a threshold value for the prevalence of avian influenza and investigate the local or global asymptotical stability of each equilibrium of these systems by using linear analysis technique or combining Liapunov function method and LaSalle's invariance principle, respectively. Moreover, we give necessary and sufficient conditions for the occurrence of periodic solutions in the avian influenza system with Allee effect of the avian population. Numerical simulations are also presented to illustrate the theoretical results.
2024-09-02 | BIOMD0000000708 | BioModels
Project description:Sanhong Liu, Shigui Ruan & Xinan Zhang. Nonlinear dynamics of avian influenza epidemic models. Mathematical Biosciences 283 (2017).
Avian influenza is a zoonotic disease caused by the transmission of the avian influenza A virus, such as H5N1 and H7N9, from birds to humans. The avian influenza A H5N1 virus has caused more than 500 human infections worldwide with nearly a 60% death rate since it was first reported in Hong Kong in 1997. The four outbreaks of the avian influenza A H7N9 in China from March 2013 to June 2016 have resulted in 580 human cases including 202 deaths with a death rate of nearly 35%. In this paper, we construct two avian influenza bird-to-human transmission models with different growth laws of the avian population, one with logistic growth and the other with Allee effect, and analyze their dynamical behavior. We obtain a threshold value for the prevalence of avian influenza and investigate the local or global asymptotical stability of each equilibrium of these systems by using linear analysis technique or combining Liapunov function method and LaSalle's invariance principle, respectively. Moreover, we give necessary and sufficient conditions for the occurrence of periodic solutions in the avian influenza system with Allee effect of the avian population. Numerical simulations are also presented to illustrate the theoretical results.
2024-09-02 | BIOMD0000000709 | BioModels
Project description:A century ago, influenza A virus (IAV) infection caused the 1918 flu pandemic and killed an estimated 20-40 million people. Pandemic IAV outbreaks occur when strains from animal reservoirs acquire the ability to infect and spread among humans. The molecular details of this species barrier are incompletely understood. We combined metabolic pulse labeling and quantitative shotgun proteomics to globally monitor protein synthesis upon infection of human cells with a human- and a bird-adapted IAV strain. While production of host proteins was remarkably similar, we observed striking differences in the kinetics of viral protein synthesis over the course of infection. Most importantly, the matrix protein M1 was inefficiently produced by the bird-adapted strain at later stages. We show that impaired production of M1 from bird-adapted strains is caused by increased splicing of the M segment RNA to alternative isoforms. Experiments with reporter constructs and recombinant influenza viruses revealed that strain-specific M segment splicing is controlled by the 3’ splice site and functionally important for permissive infection. Independent in silico and biochemical evidence shows that avian-adapted M segments have evolved different conserved RNA structure features than human-adapted sequences. Thus, our data identifies M segment RNA splicing as a viral determinant of host range.
2019-11-11 | PXD015475 | Pride
Project description:A century ago, influenza A virus (IAV) infection caused the 1918 flu pandemic and killed an estimated 20-40 million people. Pandemic IAV outbreaks occur when strains from animal reservoirs acquire the ability to infect and spread among humans. The molecular details of this species barrier are incompletely understood. We combined metabolic pulse labeling and quantitative shotgun proteomics to globally monitor protein synthesis upon infection of human cells with a human- and a bird-adapted IAV strain. While production of host proteins was remarkably similar, we observed striking differences in the kinetics of viral protein synthesis over the course of infection. Most importantly, the matrix protein M1 was inefficiently produced by the bird-adapted strain at later stages. We show that impaired production of M1 from bird-adapted strains is caused by increased splicing of the M segment RNA to alternative isoforms. Experiments with reporter constructs and recombinant influenza viruses revealed that strain-specific M segment splicing is controlled by the 3’ splice site and functionally important for permissive infection. Independent in silico and biochemical evidence shows that avian-adapted M segments have evolved different conserved RNA structure features than human-adapted sequences. Thus, our data identifies M segment RNA splicing as a viral determinant of host range.
2019-11-11 | PXD015474 | Pride
Project description:Influenza in Bird Feces
| PRJEB87825 | ENA
Project description:Establishing protocol for sequencing HA, NA and M segments Influenza A (H1N1 & H3N2) from wastewater.
| PRJEB85534 | ENA
Project description:Background：Dendritic cells (DCs), have the most important antigen presenting ability and played an irreplaceable role in recognizing and clearing virus. Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. MicroRNA, small non-coding RNAs, that can regulate dendritic cells to inhibit the infection and replication of avian influenza virus. Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. Results： Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. First, we found that both active and inactive H9N2 AIV enhance the ability of DCs to present antigens and activate T lymphocytes. Next, total microarray analyses suggested that H9N2 AIV stimulation involved in protein localization, nucleotide binding and leukocyte transendothelial migration and MAPK signal pathways. Moreover, we construct 551 transcription factor (TF)-microRNA-mRNA loops based on the above analyses. Furthermore, we found that HA fragment could not activate DCs, while truncated HA highly increased the immune function of DCs by activating ERK and STAT3 signal pathway. Last, our insight research not only gained that gga-miR1644 might target to MBNL2 to enhanced avian DCs in inhibiting virus replication, but also suggested that gga-miR6675 target to the NLS of PB1 to trigger the silencing of PB1 genes and lead to inhibition of H9N2 avian influenza viral replication. All together, our innovative research will shed new light on the roles of avian microRNA in evoking avian DCs and inhibiting virus replication, which will suggest new strategies to combat avian influenza virus.
2017-07-08 | GSE100916 | GEO
Project description:Influenza B virus (IBV) strains are one of the components of seasonal influenza vaccines in both trivalent and quadrivalent formulations. The vast majority of these vaccines are produced in embryonated chickens' eggs. While optimized backbones for vaccine production in eggs exist and are in use for influenza A viruses, no such backbones exist for IBVs, resulting in unpredictable production yields. To generate an optimal vaccine seed virus backbone, we have compiled a panel of 71 IBV strains from 1940 to present day, representing the known temporal and genetic variability of IBV circulating in humans. This panel contains strains from the B/Victoria/2/87-like lineage, B/Yamagata/16/88-like lineage and the ancestral lineage that preceded their split to provide a diverse set that would help to identify a suitable backbone which can be used in combination with hemagglutinin (HA) and neuraminidase (NA) glycoproteins from any IBV strain to be incorporated into the seasonal vaccine. We have characterized and ranked the growth profiles of the 71 IBV strains and the best performing strains were used for co-infection of eggs, followed by serial passaging to select for high-growth reassortant viruses. After serial passaging, we selected 10 clonal isolates based on their growth profiles assessed by hemagglutination and plaque-forming units. We then generated reverse genetics systems for the three clones that performed best in growth curves. The selected backbones were then used to generate different reassortant viruses with HA/NA combinations from high and low titer yielding wild type IBV. When the growth profiles of the recombinant reassortant viruses were tested, the low titer yielding HA/NA viruses with the selected backbones yielded higher titers similar to those from high titer yielding HA/NA combinations. The use of these IBV backbones with improved replication in eggs might increase yields for the influenza B virus components of seasonal influenza virus vaccines.
2023-03-10 | PXD036269 | Pride
Project description:Recent avian and swine-origin influenza virus outbreaks illustrate the ongoing threat of influenza pandemic. New vaccines that offer accelerated production and broader, more universal protection against drifted and shifted strains are needed. Here, we investigated a multivalent PMED DNA vaccine for the ability to induce antibody and T cell responses against four HA antigens, nucleoprotein and the ectodomain of M2 (M2e).
2016-07-31 | GSE77824 | GEO