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ABSTRACT: Enterovirus D68 viruses from 2018 outbreak in USA

PROVIDER: PRJNA532464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8899720_1.fastq.gz	Fastqsanger.gz
	SRR8899720_2.fastq.gz	Fastqsanger.gz
	SRR8899711_1.fastq.gz	Fastqsanger.gz
	SRR8899711_2.fastq.gz	Fastqsanger.gz
	SRR8899721_1.fastq.gz	Fastqsanger.gz

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Recent clinical isolates of enterovirus D68 have increased replication and induce enhanced epithelial immune response compared to the prototype Fermon strain.

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.

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Tissue tropism and host response: similarities and differences between enteric and respiratory enteroviruses

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.

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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.

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