Ontology highlight
ABSTRACT:
PROVIDER: PRJNA431431 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6511980_1.fastq.gz | Fastqsanger.gz | |||
| SRR6511980_2.fastq.gz | Fastqsanger.gz | |||
| SRR6511981_1.fastq.gz | Fastqsanger.gz | |||
| SRR6511981_2.fastq.gz | Fastqsanger.gz | |||
| SRR6511982_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
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Project description:Infectious pancreatic necrosis virus (IPNV) is an aquatic virus that causes acute infection in freshwater and marine fish. The stage-specific expression of TNFα regulates Bad/Bid-mediated apoptosis and RIP1/ROS-mediated secondary necrosis in IPNV-infected fish cells. Using microRNA microarray and real-time quantitative PCR assays, the expression patterns of microRNA were characterized in different replication stages of IPNV or stimulation of LPS.
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Project description:Infectious pancreatic necrosis virus (IPNV) is an aquatic virus that causes acute infection in freshwater and marine fish. The stage-specific expression of TNFα regulates Bad/Bid-mediated apoptosis and RIP1/ROS-mediated secondary necrosis in IPNV-infected fish cells. Using microRNA microarray and real-time quantitative PCR assays, the expression patterns of microRNA were characterized in different replication stages of IPNV or stimulation of LPS. Two-condition experiment, normal vs IPNV-infected cells (at 6, 12 or 24 hr post-infection), or normal vs LPS-stimulated cells (at 6, 12 or 24 h post-treatment).
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Project description:We applied numerical ecology methods to data produced with a human intestinal tract-specific phylogenetic microarray (the Aus-HIT Chip) to examine the biogeography of mucosa-associated bacteria along the human colon. The microbial DNA associated with matched biopsy tissue samples taken from the cecum, transverse colon, sigmoid colon and rectum of 10 healthy patients was examined. Consistent with previous studies, the profiles revealed a marked inter-subject variability; however, the numerical ecology methods of analysis allowed the subtraction of the subject effect from the data and revealed, for the first time, evidence of a longitudinal gradient for specific microbes along the colorectum: with Streptococcus, Comamonadaceae, Enterococcus and Lactobacillus in greatest abundance at the cecum, with a gradual decline in their relative abundance through to the rectum. Conversely, the analyses suggest that members of the Enterobacteriaceae increase in relative abundance towards the rectum. These differences were validated by quantitative PCR. We were also able to identify significant differences in the profiles, especially for the Streptococci, on the basis of gender. The results derived by these multivariate analyses are biologically intuitive, and suggestive that the biogeography of the colonic mucosa can be monitored for changes via cross-sectional and/or inception cohort studies.
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Project description:Heldt2012 - Influenza Virus Replication
The model describes the life cycle of influenza A virus in a mammalian cell including the following steps: attachment of parental virions to the cell membrane, receptor-mediated endocytosis, fusion of the virus envelope with the endosomal membrane, nuclear import of vRNPs, viral transcription and replication, translation of the structural viral proteins, nuclear export of progeny vRNPs and budding of new virions. It also explicitly accounts for the stabilization of cRNA by viral polymerases and NP and the inhibition of vRNP activity by M1 protein binding. In short, the model focuses on the molecular mechanism that controls viral transcription and replication.
This model is described in the article:
Modeling the intracellular dynamics of influenza virus replication to understand the control of viral RNA synthesis.
Heldt FS, Frensing T, Reichl U.
J Virol.
Abstract:
Influenza viruses transcribe and replicate their negative-sense RNA genome inside the nucleus of host cells via three viral RNA species. In the course of an infection, these RNAs show distinct dynamics, suggesting that differential regulation takes place. To investigate this regulation in a systematic way, we developed a mathematical model of influenza virus infection at the level of a single mammalian cell. It accounts for key steps of the viral life cycle, from virus entry to progeny virion release, while focusing in particular on the molecular mechanisms that control viral transcription and replication. We therefore explicitly consider the nuclear export of viral genome copies (vRNPs) and a recent hypothesis proposing that replicative intermediates (cRNA) are stabilized by the viral polymerase complex and the nucleoprotein (NP). Together, both mechanisms allow the model to capture a variety of published data sets at an unprecedented level of detail. Our findings provide theoretical support for an early regulation of replication by cRNA stabilization. However, they also suggest that the matrix protein 1 (M1) controls viral RNA levels in the late phase of infection as part of its role during the nuclear export of viral genome copies. Moreover, simulations show an accumulation of viral proteins and RNA toward the end of infection, indicating that transport processes or budding limits virion release. Thus, our mathematical model provides an ideal platform for a systematic and quantitative evaluation of influenza virus replication and its complex regulation.
With the current parameter set, the model reproduces an infection at a multiplicity of infection (MOI) of 10. Figure 2A of the paper is reproduced here, with parameters kDegRnp and kSynP changed to zeros.
Initial conditions and parameter changes that were used to obtain specific figures in the article can be found in Table A2.
The model has the correct value for kAttLo as 4.55e-04. The value of this parameter mentioned as 4.55e-02 in Table 1 of the paper is incorrect. This is checked with the author.
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2024-09-02 | BIOMD0000000463 | BioModels