Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Signal sequences in the viral genome regulate the generation of copy-back defective viral genomes

ABSTRACT: Signal sequences in the viral genome regulate the generation of copy-back defective viral genomes

PROVIDER: PRJNA473161 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7221080_1.fastq.gz	Fastqsanger.gz
	SRR7221080_2.fastq.gz	Fastqsanger.gz
	SRR7221090_1.fastq.gz	Fastqsanger.gz
	SRR7221090_2.fastq.gz	Fastqsanger.gz
	SRR7221081_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Signal sequences in the viral genome regulate the generation of copy-back defective viral genomes

Project description:We developed VODKA (Viral Opensource DVG Key Algorithm) to identify cbDVGs from RNA-Seq data from infected samples and used these DVG sequences to identify signals that regulate cbDVG generation. We applied VODKA to datasets from RSV-positive patients. VODKA identified common cbDVGs across multiple samples in both patients, and predicted specific genomic loci that mediate cbDVG formation.

2019-03-19 | GSE114948 | GEO

Recognition of copy-back defective interfering rabies virus genomes by RIG-I triggers efficient immune response against vaccine strains

Project description:Using next-generation sequencing (NGS) combined with bioinformatics tools, we characterized two major 5’copy-back defective interfering (5’cb DI) genomes generated during SAD replication. Furthermore, we identified a specific interaction of 5’cb DI genomes and RIG-I that correlated with a high stimulation of the type I IFN signaling

2024-03-22 | GSE196051 | GEO

Defective viral genomes determine respiratory syncytial virus disease severity in adult and children cohorts

Project description:Defective viral genomes of the copy-back type (cbDVGs) are generated during RSV infectin and are suggested to impact the clinical outcome. Here in this study we selected the nasal secretions from 13 hospitalized pediatric pateints, including both cnDVG+ and cbDVG-, to perform RNA-seq to understand the impact of cbDVGs on patient transcriptome.

2021-01-25 | GSE146925 | GEO

Applying defective interfering viral genome bioinformatics for detection of coronavirus subgenomic RNAs

Project description:Coronavirus RNA-dependent RNA polymerases produce subgenomic RNAs (sgRNAs) that encode viral structural and accessory proteins. The kinetics and efficiency of sgRNAs production during viral replication in different cell types or sgRNA transcription by individual viral strains or variants are yet to be studied to shed light on fundamental mechanisms necessary for viral replication. User-friendly bioinformatic tools to detect and quantify sgRNA production are urgently needed to study a growing number of next-generation sequencing (NGS) data of SARS-CoV-2. Starting from DI-tector, a bioinformatic tool for the detection of viral defective interfering genomes, here we introduced sgDI-tector to identify and quantify sgRNA in SARS-CoV-2 NGS data. This new tool allowed detection of sgRNA without initial knowledge of the transcription-regulatory sequences. As a proof of principle, we analyzed new data sets and successfully detected the nested set of sgRNAs produced with the ranking M>ORF3a>N>ORF6>ORF7a>ORF8>S>E>ORF7b. Our study also compared, for the first time for SARS-CoV-2, the level of sgRNA production with other types of viral RNA products such as defective interfering viral genomes.

2021-12-28 | GSE180632 | GEO

A measles virus collective infectious unit that caused lethal human brain disease includes many locally restricted and few widespread copy-back defective genomes

Project description:During virus replication in cultured cells, copy-back defective viral genomes (cbDVG) can arise. CbDVG are powerful inducers of innate immune responses in vitro, but their occurrence and impact on natural infections of human hosts remain poorly defined. We asked whether cbDVG were generated in the brain of a patient who succumbed to subacute sclerosing panencephalitis (SSPE) about 20 years after acute measles virus (MeV) infection. Previous analyses of 13 brain specimens of this patient indicated that a collective infectious unit (CIU) drove lethal MeV spread. In this study, we identified 276 replication-competent cbDVG species, each present in over 100 copies in the brain. Six species were detected in multiple forebrain locations, implying that they travelled long-distance with the CIU. The cbDVG to full-length genomes ratio was often close to 1 (0.6-1.74). Most cbDVG were 324-2000 bases in length, corresponding to 2-12% of the full-length genome; all are predicted to have complementary terminal sequences. If improperly encapsidated, these sequences have the potential to form double-stranded structures that can induce innate immune responses. To assess this, we examined the transcriptome of all brain specimens. Several interferon- and inflammatory response genes were upregulated, but upregulation levels did not correlate with cbDVG levels in the specimens. Thus, the CIU that drove MeV pathogenesis in this brain includes, in addition to two complementary full-length genome populations, many locally restricted and few widespread cbDVG species. The widespread cbDVG species may have been positively selected but how they impacted pathogenesis remains to be determined.

2024-10-01 | GSE272560 | GEO

meg-3 meg-4 mutants are defective in exogenous RNAi signal amplification

Project description:meg-3 meg-4 mutants are defective in exogenous RNAi signal amplification

| PRJNA555887 | ENA

Generation and functional analysis of defective viral genomes during SARS-CoV-2 infection

Project description: In this study, we elucidated defective viral genome generation in SARS-CoV-2 and its relationship with host antiviral immune response. We observed DVGs ubiquitously from RNA-seq datasets of in vitro infections and autopsy lung tissues of COVID-19 patients.

2023-07-05 | GSE222381 | GEO

A specific sequence in the genome of respiratory syncytial virus regulates the generation of copy-back defective viral genomes.

Project description:Defective viral genomes of the copy-back type (cbDVGs) are the primary initiators of the antiviral immune response during infection with respiratory syncytial virus (RSV) both in vitro and in vivo. However, the mechanism governing cbDVG generation remains unknown, thereby limiting our ability to manipulate cbDVG content in order to modulate the host response to infection. Here we report a specific genomic signal that mediates the generation of a subset of RSV cbDVG species. Using a customized bioinformatics tool, we identified regions in the RSV genome frequently used to generate cbDVGs during infection. We then created a minigenome system to validate the function of one of these sequences and to determine if specific nucleotides were essential for cbDVG generation at that position. Further, we created a recombinant virus unable to produce a subset of cbDVGs due to mutations introduced in this sequence. The identified sequence was also found as a site for cbDVG generation during natural RSV infections, and common cbDVGs originated at this sequence were found among samples from various infected patients. These data demonstrate that sequences encoded in the viral genome determine the location of cbDVG formation and, therefore, the generation of cbDVGs is not a stochastic process. These findings open the possibility of genetically manipulating cbDVG formation to modulate infection outcome.

| S-EPMC6504078 | biostudies-literature

Correction: A specific sequence in the genome of respiratory syncytial virus regulates the generation of copy-back defective viral genomes.

Project description:[This corrects the article DOI: 10.1371/journal.ppat.1007707.].

| S-EPMC6776294 | biostudies-literature

Applying defective interfering viral genome bioinformatics for detection of coronavirus subgenomic RNAs

Project description:Applying defective interfering viral genome bioinformatics for detection of coronavirus subgenomic RNAs

| PRJNA749002 | ENA