Ontology highlight
ABSTRACT:
PROVIDER: PRJNA421629 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8949705_1.fastq.gz | Fastqsanger.gz | |||
| SRR8949705_2.fastq.gz | Fastqsanger.gz | |||
| SRR8945328_subreads.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Parasitic elements of the viral population which are unable to replicate on their own yet rise to high frequencies, defective interfering particles are found in a variety of different viruses. Their presence is associated with a loss of population fitness, both through the depletion of key cellular resources and the stimulation of innate immunity. For influenza A virus, these particles contain large internal deletions in the genomic segments which encode components of the heterotrimeric polymerase. Using a library-based approach, we comprehensively profile the growth and replication of defective species, demonstrating they possess an advantage during genome replication, and that exclusion during packaging reshapes population composition in a manner consistent with their final, observed, distribution in natural populations. We find that innate immunity is not linked to the size of a deletion; however, replication of defective segments can enhance their immunostimulatory properties. Overall, our results address several key questions in defective influenza A virus biology, and the methods we have developed to answer those questions may be broadly applied to other defective viruses.
2021-11-17 | GSE183442 | GEO
Project description:This a model from the article:
Modeling defective interfering virus therapy for AIDS: conditions for DIV
survival.
Nelson GW, Perelson AS. Math Biosci
1995 Feb;125(2):127-53 7881191
,
Abstract:
The administration of a genetically engineered defective interfering virus (DIV)
that interferes with HIV-1 replication has been proposed as a therapy for HIV-1
infection and AIDS. The proposed interfering virus, which is designed to
superinfect HIV-1 infected cells, carries ribozymes that cleave conserved
regions in HIV-1 RNA that code for the viral envelope protein. Thus DIV
infection of HIV-1 infected cells should reduce or eliminate viral production by
these cells. The success of this therapeutic strategy will depend both on the
intercellular interaction of DIV and HIV-1, and on the overall dynamics of virus
and T cells in the body. To study these dynamical issues, we have constructed a
mathematical model of the interaction of HIV-1, DIV, and CD4+ cells in vivo. The
results of both mathematical analysis and numerical simulation indicate that
survival of the engineered DIV purely on a peripheral blood HIV-1 infection is
unlikely. However, analytical results indicate that DIV might well survive on
HIV-1 infected CD4+ cells in lymphoid organs such as lymph nodes and spleen, or
on other HIV-1 infected cells in these organs.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Nelson GW, Perelson AS. (1995) - version=1.0
The original CellML model was created by:
Ethan Choi
mcho099@aucklanduni.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230033 | BioModels
Project description:This a model from the article:
Modeling defective interfering virus therapy for AIDS: conditions for DIV
survival.
Nelson GW, Perelson AS. Math Biosci
1995 Feb;125(2):127-53 7881191
,
Abstract:
The administration of a genetically engineered defective interfering virus (DIV)
that interferes with HIV-1 replication has been proposed as a therapy for HIV-1
infection and AIDS. The proposed interfering virus, which is designed to
superinfect HIV-1 infected cells, carries ribozymes that cleave conserved
regions in HIV-1 RNA that code for the viral envelope protein. Thus DIV
infection of HIV-1 infected cells should reduce or eliminate viral production by
these cells. The success of this therapeutic strategy will depend both on the
intercellular interaction of DIV and HIV-1, and on the overall dynamics of virus
and T cells in the body. To study these dynamical issues, we have constructed a
mathematical model of the interaction of HIV-1, DIV, and CD4+ cells in vivo. The
results of both mathematical analysis and numerical simulation indicate that
survival of the engineered DIV purely on a peripheral blood HIV-1 infection is
unlikely. However, analytical results indicate that DIV might well survive on
HIV-1 infected CD4+ cells in lymphoid organs such as lymph nodes and spleen, or
on other HIV-1 infected cells in these organs.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Nelson GW, Perelson AS. (1995) - version=1.0
The original CellML model was created by:
Ethan Choi
mcho099@aucklanduni.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230081 | BioModels
Project description:Influenza defective interfering virus promotes multiciliated cell differentiation and reduces the inflammatory response in mice
| PRJNA777796 | ENA
Project description:The aim of this experiment was to analyse the innate immune response in alveolar cells after different nanoparticle formulations are delivered intranasally in 50 µl PBS with or without 1 µg Sendai virus Defective Interfering RNA
2021-11-22 | GSE183892 | GEO
Project description:Host-influenza virus interplay at the transcript level has been extensively characterized in epithelial cells. Yet, there are no studies that simultaneously characterize human host and influenza A virus (IAV) genomes. We infected human bronchial epithelial BEAS-2B cells with two seasonal IAV/H3N2 strains, Brisbane/10/07 and Perth/16/09 (reference strains for past vaccine seasons) and the well-characterized laboratory strain Udorn/307/72. Strand-specific RNA-seq of the infected BEAS-2B cells allowed for simultaneous analysis of host and viral transcriptomes, in addition to pathogen genomes, to reveal changes in mRNA expression and alternative splicing (AS). In general, patterns of global and immune gene expression induced by the three IAVs were mostly shared. However, AS of host transcripts and small nuclear RNAs differed between the seasonal and laboratory strains. Analysis of viral transcriptomes showed deletions of the polymerase components (defective interfering (DI)-like RNAs) within the genome. Surprisingly, we found that the neuraminidase gene undergoes AS, and that the splicing event differs between seasonal and laboratory strains. Our findings reveal novel elements of the host-virus interaction and highlight the importance of RNA-seq in identifying molecular changes at the genome level that may contribute to shaping RNA-based innate immunity.
2018-05-25 | GSE61517 | GEO
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.
This model is hosted on BioModels Database
and identified
by: MODEL1307270000
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2024-09-02 | BIOMD0000000463 | BioModels
Project description:Although accumulating evidence has shown that long non-coding RNAs (lncRNAs) are involved in multiple biological processes, considerably less is known regarding their functions in influenza A virus (IAV) replication. Here, lncRNA expression profiles were determined by RNA sequencing in three pairs of influenza virus A/Puerto Rico/8/34 (H1N1)-infected or uninfected A549 cells.
2023-03-31 | GSE208546 | GEO
Project description:Virus and host factors contribute to cell-to-cell variation in viral infection and determine the outcome of the overall infection. However, the extent of the variability at the single cell level and how it impacts virus-host interactions at a systems level are not well understood. To characterize the dynamics of viral transcription and host responses, we used single-cell RNA sequencing to quantify at multiple time points the host and viral transcriptomes of human A549 cells and primary bronchial epithelial cells infected with influenza A virus. We observed substantial variability of viral transcription between cells, including the accumulation of defective viral genomes (DVGs) that impact viral replication. We show a correlation between DVGs and viral-induced variation of the host transcriptional program and an association between differential induction of innate immune response genes and attenuated viral transcription in subpopulations of cells. These observations at the single cell level improve our understanding of the complex virus-host interplay during influenza infection.
2019-12-10 | GSE118773 | GEO
Project description:Long non-coding RNAs (lncRNAs) are a new arm of gene regulatory mechanism as discovered by sequencing techniques and follow-up functional studies. There are only few studies on lncRNAs as related to gene expression regulation and anti-viral activity during influenza virus infection. We sought to identify and characterize lncRNAs involved in influenza virus replication. In the current study, we identified dys-regulated lncRNAs in influenza virus-infected human lung epithelial A549 cells using RNA sequencing in A549 cells.
2018-10-12 | GSE121155 | GEO