Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1173516 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31013000_1.fastq.gz | Fastqsanger.gz | |||
| SRR31013000_2.fastq.gz | Fastqsanger.gz | |||
| SRR31013001_1.fastq.gz | Fastqsanger.gz | |||
| SRR31013001_2.fastq.gz | Fastqsanger.gz | |||
| SRR31013002_1.fastq.gz | Fastqsanger.gz |
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Project description:With the near eradication of poliovirus due to global vaccination campaigns, attention has shifted to other enteroviruses that can cause polio-like paralysis syndrome (now termed acute flaccid myelitis (AFM)). In particular, enterovirus D68 (EV-D68) is believed to be the main driver of epidemic outbreaks of AFM in recent years, yet not much is known about EV-D68 host interactions. EV-D68 is a respiratory virus but, in rare cases, can spread to the central nervous system to cause severe neuropathogenesis. We use genome-scale CRISPR screens to identify genes important for EV-D68 infection. A549 and U87-MG cells were stably transduced with lentiCas9-Blast (Addgene, #52962) and subsequently selected using Blasticidin. Then, 300 million cells that constitutively express Cas9 were transduced with lentiGuide-Puro from the Brunello library (MOI 0.3). Cells were then selected with puromycin, expanded to 3 billion cells, and then pooled together and cryofrozen in aliquots. One hundred million cells were thawed constituting over 1000× genome coverage worth of mutagenized library,expanded, and seeded for the screens. Each screen had over 500x genome coverage. The cells were infected with EV-D68 IL (BEI USA/2014/18952) (MOI 0.1). Virus-resistant colonies were harvested. The uninfected reference used was the unselected starting population. The unselected and selected cells were both processed with QIAamp DNA columns to purify the gDNA. A first round of PCR was used to amplify the guide RNA sequences encoded in the gDNA, followed by a second round of PCR to add the barcodes/adapters for amplicon sequencing. 2% agarose gels and a QIAquick gel extraction kit were used to purify the amplicons. The amplicons were then subjected to next-generation sequencing on a HiSeq instrument lane (Illumina) via Novogene.
2025-02-25 | E-MTAB-14765 | biostudies-arrayexpress
Project description:Enteroviruses (EVs) are one of the most prevalent viruses worldwide. They are characterised by a high genetic and phenotypic diversity, being able to cause a plethora of symptoms. EV-D68, a respiratory EV, and EV-D94, an enteric EV, represent an interesting paradigm of EV tropism heterogeneity. These are closely related viruses, belonging to the same species, but with distinct phenotypic features. Here, we used these two viruses as well as relevant tissue culture models mimicking the respiratory and intestinal epithelia, to highlight key distinctive features of enteric and respiratory EVs. We emphasize the critical role of temperature in restricting the tissue tropism of EV-D68 and the limited replication of EV-D94 in small airway tissues. In parallel, using transcriptomic analysis, we uncover fundamental differences between intestinal and respiratory tissues, in their steady-state as well as in response to infection. Intestinal tissues are more immunotolerant than respiratory tissues both in absence and presence of infection and they present higher turnover. Finally, we highlight the different strategies applied by EV-D94 and EV-D68 towards the host antiviral response in intestinal and respiratory tissues. In summary, our study provides an insightful characterization of the differential pathogenesis of EV-D68 and EV-D94 and the interplay with their main target tissues.
2022-06-23 | GSE184488 | GEO
Project description:In 2014, enterovirus D68 (EV-D68), previously associated primarily with mild respiratory illness, caused a large outbreak of severe respiratory illness and, in rare instances, paralysis. We compared viral binding and replication of eight recent EV-D68 clinical isolates and the prototype Fermon strain from 1962 in cultured HeLa cells and differentiated human primary bronchial epithelial cells (BEC) to understand the possible reasons for the change in virus pathogenicity. We found no significant differences in binding or replication in HeLa cell cultures between the recent clinical isolates. However, in HeLa cells, Fermon had significantly greater (1.5-2 log) binding and virus progeny yields but a similar level of replication (~2-log increase in viral RNA from 2h to 24h post infection) compared to recent isolates. In differentiated BECs, Fermon and the recent EV-D68 isolates had similar levels of binding; however, the recent isolates produced 1-2-log higher virus progeny yields than Fermon due to increased replication. We then utilized RNA-seq to define the transcriptional responses in BECs infected with four recent EV-D68 isolates, representing major phylogenetic clades, and Fermon strain. All the tested clinical isolates induced similar responses in BECs; however, numerous upregulated genes in antiviral and pro-inflammatory response pathways were identified when comparing the response to clinical isolates versus Fermon. These results indicate that the recent emergence in severe EV-D68 cases could be explained by increased replication efficiency and enhanced inflammatory response induced by newly emerged clinical isolates.
2023-07-06 | GSE233630 | GEO
Project description:The mechanisms by which enteroviruses, particularly enterovirus D-68 (EV-D68) and enterovirus A-71 (EV-A71), contribute to acute flaccid myelitis (AFM), a severe neurological condition characterized by sudden muscle weakness and paralysis, remain poorly understood. To investigate the cellular tropism and infection dynamics of these enteroviruses, we utilized human spinal cord organoids (hSCOs) derived from induced pluripotent stem cells (iPSCs). We performed single-cell RNA sequencing (scRNA-seq) to profile the cellular composition of hSCOs and identify infected cell types post-infection. We found that hSCOs exhibit a diverse cellular landscape, including neurons, astrocytes, oligodendrocyte progenitor cells (OPCs), and multipotent glial progenitor cells (mGPCs), with astrocytes predominant in earlier developmental stages and neurons more abundant in later stages. Upon infection with two EV-D68 strains (US/IL/14-18952 and US/CO/18-23089) and one EVA71 strain (Tainan/4643/1998), we observed distinct viral tropism. EV-D68-18952 showed a significant increase in infected neurons, while EV-D68-23089 exhibited higher infection rates in cycling astrocytes and OPCs. In contrast, EVA71 demonstrated a broader tropism, with a statistically significant increase in infected mGPCs, suggesting enhanced infection efficiency across multiple cell types. These findings provide novel insights into the cell-type specificity of EV-D68 and EVA71 in the spinal cord, offering a deeper understanding of potential mechanisms underlying AFM pathogenesis. Understanding the dynamics of infection at single-cell resolution will inform future therapeutic strategies aimed at mitigating the neurological impact of enteroviral infections.
2025-07-30 | GSE292051 | GEO
Project description:Febrile patients PCR positive for H1N1 swine flu, seasonal H1N1 and seasonal H3N2 in nasal swabs and controls consisting of febrile patients with rhinovirus infection or febrile patients of non-viral etiology (nasal swabs PCR negative for common respiratory viruses and blood PCR negative for dengue and parvovirus B19) were assessed consecutively for global transcriptional changes in whole blood
2014-04-01 | GSE29385 | GEO
Project description:Respiratory viruses pose an ongoing threat to human health, with excessive cytokine secretion playing a critical role in severe illness and mortality. However, the complex relationship between cytokine secretion and viral infection remains poorly understood. Here, we have unraveled the role of cxcl8 as an early response gene to respiratory EV-D68 infection. The upregulation of CXCL8 by viral infection is found to be crucial for EV-D68 replication. Importantly, silencing CXCL8 or its receptors, CXCR1/2, significantly impedes EV-D68 replication. Upon recognition of CXCL8 by CXCR1/2, the MAPK pathway is activated, facilitating the translocation of the essential host cofactor hnRNP K from the nucleus to the cytoplasm. This translocation enhances the recognition of viral RNA by hnRNP K in the cytoplasm, promoting the functionality of the 5’UTR region in the viral genome. Interestingly, the VP4 structural protein of EV-D68 contains a mimic motif of human immunoreceptor tyrosine-based activation motif (ITAM) that interacts with syk and triggers the PI3K/AKT signaling pathway, resulting in elevated CXCL8 gene expression for viral replication. Moreover, our investigations reveal the conservation and significance of the CXCL8 signaling pathway across various prominent human respiratory viruses, including SARS-CoV-2, influenza, and rhinovirus. In summary, our findings unveil a paradigmatic mechanism through which respiratory viruses exploit cytokine-mediated intercellular communication to transmit signals that optimize viral replication. This deepens our understanding of the shared evolutionary strategies employed by respiratory viruses and opens up new avenues for the development of broad-spectrum antiviral drugs targeting respiratory pathogens.
2024-11-22 | GSE273371 | GEO
Project description:Febrile patients PCR positive for H1N1 swine flu, seasonal H1N1 and seasonal H3N2 in nasal swabs and controls consisting of febrile patients with rhinovirus infection or febrile patients of non-viral etiology (nasal swabs PCR negative for common respiratory viruses and blood PCR negative for dengue and parvovirus B19) were assessed consecutively for global transcriptional changes in whole blood Peripheral whole blood collected in PAX-gene tubes and extracted for total RNA
2014-04-01 | E-GEOD-29385 | biostudies-arrayexpress