Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17205223_1.fastq.gz | Fastqsanger.gz | |||
| SRR17205223_2.fastq.gz | Fastqsanger.gz | |||
| SRR17205224_1.fastq.gz | Fastqsanger.gz | |||
| SRR17205224_2.fastq.gz | Fastqsanger.gz | |||
| SRR17205225_1.fastq.gz | Fastqsanger.gz |
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Project description:Viruses make extensive use of host cell machinery, however, most systematic studies of virus-host interactions focused on proteins with less attention to nucleic acids. RNA plays important roles in storing, conveying, and regulating genetic information. Our understanding of functional interactions between viral and host RNA is dominated by interactions with micro-RNAs (miRNAs), such as the interaction between hepatitis C virus (HCV) and the liver specific miR-122, critical for viral replication. Methodological developments, however, allow for broader exploration of the RNA interaction landscape beyond that of miRNAs. We here set out to identify virus-host RNA interactions by optimizing RNA antisense purification to systematically map RNA-RNA interactions (RAP-RNA) for viral RNA. After using the HCV/miR-122 interaction for validation, we applied RAP-RNA to determine the RNA interactomes for three important human pathogens; HCV, yellow fever virus (YFV) and chikungunya virus (CHIKV). Comparing virus-host RNA interactomes, we observed patterns of mRNAs encoding factors involved in translation and the proteasome, mitochondrial (mt)RNAs, small nucleolar (sno)RNAs and small nuclear (sn)RNAs, thereby providing a more comprehensive understanding of cellular RNA interactions for RNA viruses. Experimental targeting of selected HCV interactors did not lead to significant impact on viral infection, suggesting that the majority of virus-host RNA interactions are not critical for the virus. In contrast, transcription data were consistent with a possible role in viral stabilization of host RNA interactors. These findings may guide future research directions, e.g., for the role of snoRNAs and snRNAs in viral RNA regulation, with potential to provide further insight to viral exploitation of host factors.
2026-04-29 | GSE309201 | GEO
Project description:We used 4C sequencing technology for high-throughput profiling of HHV6A integration in both HEK293T cells and SMC cells. We identified genome-wide host-virus and virus-virus interactions profiles.
2020-12-09 | GSE162821 | GEO
Project description:Archaeal viruses display unusually high genetic and morphologic diversity. The Sulfolobus islandicus Rod Shaped Virus 2 (SIRV2) is a model to study virus-host interactions in Archaea. It is a lytic virus that exploits a unique egress mechanism based on formation of remarkable pyramidal structures on the host cell envelope. The hyperthermophilic Sulfolobus islandicus LAL14/1 is the natural host for SIRV2. RNA was isolated at 0,1,2,3,5,7 and 9 hours after SIRV2 infection of two S.islandicus cultures and analysed with whole transcriptome sequencing (RNAseq). As a control RNA was isolated at the same time points from two uninfected cultures.
2013-05-25 | E-MTAB-1660 | biostudies-arrayexpress
Project description:Respiratory viral coinfections pose a substantial global health burden, yet the underlying virus–virus interactions remain incompletely understood. Here, we systematically examined the interplay among influenza A virus (IAV), SARS-CoV-2, and respiratory syncytial virus (RSV) using a reconstituted human airway epithelium model. We monitored viral replication dynamics and host transcriptional responses under both simultaneous and sequential infection conditions.
2026-01-30 | E-MTAB-16265 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs), including host miRNAs and viral miRNAs, play vital roles in regulating host-virus interactions. DNA viruses encode miRNAs that regulate the viral life cycle. However, it is generally believed that cytoplasmic RNA viruses do not encode miRNAs, owing to inaccessible cellular miRNA processing machinery. Here, we provide a comprehensive genome-wide analysis and identification of miRNAs that were derived from hepatitis A virus (HAV; Hu/China/H2/1982), which is a typical cytoplasmic RNA virus. Using deep-sequencing and in silico approaches, we identified 2 novel virally encoded miRNAs, named hav-miR-1-5p and hav-miR-2-5p. Both of the novel virally encoded miRNAs were clearly detected in infected cells. Analysis of Dicer enzyme silencing demonstrated that HAV-derived miRNA biogenesis is Dicer dependent. Furthermore, we confirmed that HAV mature miRNAs were generated from viral miRNA precursors (pre-miRNAs) in host cells. Notably, naturally derived HAV miRNAs were biologically and functionally active and induced post-transcriptional gene silencing (PTGS). Genomic location analysis revealed novel miRNAs located in the coding region of the viral genome. Overall, our results show that HAV naturally generates functional miRNA-like small regulatory RNAs during infection. This is the first report of miRNAs derived from the coding region of genomic RNA of a cytoplasmic RNA virus. These observations demonstrate that a cytoplasmic RNA virus can naturally generate functional miRNAs, as DNA viruses do. These findings also contribute to improved understanding of host-RNA virus interactions mediated by RNA virus-derived miRNAs.
2014-01-24 | GSE54368 | GEO
Project description:Coronaviruses, including SARS-CoV-2, can cause severe disease in humans, whereas reservoir hosts like Rhinolophus bats appear to remain asymptomatic for reasons that are not well-recognized. To understand how host-specific protein-protein interactions (PPIs) shape infection outcomes, we generated comparative PPI maps for SARS-CoV-2 and its close bat-originating relative, RaTG13, using affinity purification-mass spectrometry (AP-MS) in human and Rhinolophus ferrumequinum (RFe) bat cells. Our analysis revealed both conserved as well as virus- and host-specific PPIs, pointing to key interactions that regulate infection dynamics across species. SARS-CoV-2 required a non-synonymous mutation at the RNA-binding domain of the viral N protein to replicate in the RFe bat cells. Moreover, comparative analysis of the viral protein Orf9b revealed differential interactions with the human and bat mitochondrial proteins Tom70 and MTARC2, and modulating virus replication. A single residue in SARS-CoV-2 Orf9b serves as a molecular switch between these interactions, with a T72I substitution weakening Tom70 binding and reducing its ability to counteract innate immune activation. These findings demonstrate how a single-residue substitution can reshape virus-host interactions and contribute to immune evasion and host adaptation.
2026-05-13 | GSE302357 | GEO
Project description:Identifying host factors is key to understanding RNA virus pathogenicity. Besides proteins, RNAs can interact with virus genomes to impact replication. Here, we used proximity ligation sequencing to identify virus-host RNA interactions for four strains of Zika virus (ZIKV) and one strain of dengue virus (DENV-1) in human cells. We found hundreds of coding and non-coding RNAs that bind to DENV and ZIKV viruses. Host RNAs tend to bind to single-stranded regions along the virus genomes and the binding is primarily driven by hybridization energetics. We observed that virus interacting host RNAs tend to be downregulated upon virus infection and identified a conserved set of virus responders that binds to most DENV and ZIKV. Knockdown of several short non-coding RNAs, including miR19a-3p, SCARNA2 and 7SK RNA resulted in a decrease in virus growth, suggesting that they act as virus permissive factors. In addition, the 3’UTR of DYNLT1 mRNA acts as a virus restrictive factor by binding to the conserved dumbbell region on DENV and ZIKV 3’UTR to decrease virus replication. This study demonstrates that host RNAs in themselves can impact virus growth in permissive and restrictive ways, expanding our understanding of host factors and RNA-based gene regulation during virus pathogenesis.
2021-06-10 | GSE176428 | GEO