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

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

PROVIDER: PRJNA749002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15215972.fastq.gz	Fastqsanger.gz
	SRR15215973.fastq.gz	Fastqsanger.gz
	SRR15215974.fastq.gz	Fastqsanger.gz

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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

sgDI-tector: defective interfering viral genome bioinformatics for detection of coronavirus subgenomic RNAs.

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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

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Influenza defective interfering virus promotes multiciliated cell differentiation and reduces the inflammatory response in mice

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Conserved motifs in a tombusvirus polymerase modulate genome replication, subgenomic transcription, and amplification of defective interfering RNAs.

Project description: Not available

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A stable subgenomic reporter coronavirus enables transcriptional profiling of bystander cells.

Project description:Insertion of fluorescent reporter genes into viral genomes is a powerful tool for monitoring infection. In coronaviruses, this is commonly achieved by replacing accessory open reading frames, thereby deleting endogenous gene functions. An alternative strategy is to manipulate viral transcription by inserting copies of the viral transcription regulatory sequence (TRS) which drive viral subgenomic RNA transcription. However, coronavirus transcription is tightly regulated, and these modifications frequently disrupt native subgenomic RNA synthesis and attenuate viral growth. Here, we report a reporter coronavirus that overcomes these limitations. Using human coronavirus (HCoV)-OC43 as a model system, we inserted an mNeonGreen reporter between the Spike and ORF5 coding regions, engineering the TRS and surrounding sequence to minimise off-target effects to transcription. This virus is genetically stable, with wildtype growth kinetics and unaltered subgenomic RNA transcriptional ratios. We developed a flexible reverse genetics system, which allows rapid cloning and virus recover, supported by optimised HCoV-OC43 culture conditions, which support high titre stock growth, and validated analytical reagents. Our reporter virus enabled sensitive detection and isolation of infected cells, facilitating transcriptomic analyses that distinguish host responses in infected and bystander populations. Together, these tools expand the experimental utility of HCoV-OC43, an important seasonal respiratory pathogen and low containment model for betacoronavirus biology.

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Influenza defective interfering virus promotes multiciliated cell differentiation and reduces the inflammatory response in mice

Project description:Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and to induce antiviral immunity. However, the mechanisms underlying DI-mediated antiviral immunity have not been extensively explored. Here, we demonstrated interferon (IFN) independent protection conferred by influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. By integrating transcriptional and post-transcriptional regulatory data we identified unique host signatures in response to DI co-infection. DI-treated mice exhibited reduced viral transcription, less intense inflammatory and innate immune responses, and primed multiciliated cell differentiation in their lungs at an early stage of infection, even in the absence of type I or III IFNs. This increased multiciliogenesis could also be detected at the protein level by immunofluorescence staining of lung tissue from DI-treated mice. Overall, our study provides mechanistic insight into the protection mediated by DIs, implying a unifying theme involving inflammation and multiciliogenesis in maintaining respiratory homeostasis, and reveals their IFN-independent antiviral activity.

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

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

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Altered Subgenomic RNA Abundance in SARS-CoV-2 B.1.1.7 Infections

Project description:SARS-CoV-2 lineage B.1.1.7 viruses are more transmissible, may lead to greater clinical severity, and result in modest reductions in antibody neutralization. Subgenomic RNA(sgRNA) is produced by discontinuous transcription of the SARS-CoV-2 genome. Applying our tool(periscope) to ARTIC Network Nanopore genomic sequencing data from 4400 SARS-CoV-2 positive clinical samples, we show that normalised sgRNA is significantly increased in B.1.1.7(alpha) infections(n=879). This increase is seen over the previous dominant circulating UK lineage, B.1.177(n=943), which is independent of genomic reads, E-gene cycle-threshold and days since symptom onset at sampling. A noncanonical sgRNA which could represent ORF9b is found in 98.4% of B.1.1.7 SARS-CoV-2 infections compared with only 13.8% of other lineages, with a 16-fold increase in median sgRNA abundance. We demonstrate that ORF9b protein levels are increased 6-fold in B.1.1.7 compared to a B lineage virus during in vitro culture. We hypothesise that this enhanced presence of ORF9b in B.1.1.7 viruses is a direct consequence of a triple nucleotide mutation in nucleocapsid(28280:GAT>CAT,D3L) creating a transcription regulatory-like sequence complementary to a region 3’ of the genomic leader. These findings provide a unique insight into the biology of B.1.1.7 and support monitoring of sgRNA profiles in sequence data to evaluate emerging potential variants of concern.

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Overexpression of each of the 6 interfering TFs and 5 non-interfering TFs

Project description:To clarify that the interfering effect in iPS induction was not because of extraordinary gene expression which was caused by overexpression of infected genes, transcriptional profile of the cells infected six genes were analysed using microarray analysis. As result, overexpression of each of the 6 interfering TFs in NSEB5-2C did not compromise transcriptional profile compared with the five non-interfering TFs.

2011-06-07 | GSE29728 | GEO

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