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Enterovirus D68

ABSTRACT: Enterovirus D68 sequence from clinical isolates (St. Louis, 2014)

PROVIDER: PRJNA263037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1609280.fastq.gz	Fastqsanger.gz
	SRR1609280_1.fastq.gz	Fastqsanger.gz
	SRR1609280_2.fastq.gz	Fastqsanger.gz
	SRR1609271.fastq.gz	Fastqsanger.gz
	SRR1609271_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.

2023-07-06 | GSE233630 | GEO

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