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The robust inflammatory responses caused by MjHKU4r-S mediated cell fusion

ABSTRACT: The robust inflammatory responses caused by MjHKU4r-S mediated cell fusion

PROVIDER: PRJNA1258238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33413229_1.fastq.gz	Fastqsanger.gz
	SRR33413229_2.fastq.gz	Fastqsanger.gz
	SRR33413230_1.fastq.gz	Fastqsanger.gz
	SRR33413230_2.fastq.gz	Fastqsanger.gz
	SRR33413231_1.fastq.gz	Fastqsanger.gz

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The robust inflammatory responses caused by MjHKU4r-S mediated cell fusion

Project description:The Middle East Respiratory Syndrome Coronavirus (MERS-CoV) has extremely high virulence and pathogenicity in human, but some MERS-related coronaviruses (bat-CoV HKU4, bat-CoV HKU5-1/2 and MOW15-22/PnNL2018B) showed limited infectivity in human beings. Unlike previously reported MERS-related coronaviruses, the currently identified MERS-related Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) exhibited significant infectivity in human cell, organs, and hDPP4-transgenic mice. However, the detailed pathogenic features and underlying mechanisms were unknown. In virological experiments, we found MjHKU4r-CoV-1 triggered extensive syncytia formation by its spike protein (S) and caused significant inflammation responses. Herein, we use RNA sequencing (RNA-Seq) to investigate the transcriptional alterations underlying the robust inflammatory responses caused by S protein mediated syncytia formation.

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Pandemic H1N1 Influenza A Directly Induces a Robust and Acute Inflammatory Gene Signature in Primary Human Bronchial Epithelial Cells Downstream of Membrane Fusion

Project description:Pandemic H1N1 influenza A (H1N1pdm) elicits stronger pulmonary inflammation than previously circulating seasonal H1N1 influenza A (sH1N1), yet mechanisms of inflammatory activation in respiratory epithelial cells during H1N1pdm infection are unclear. We investigated host responses to H1N1pdm / sH1N1 infection and virus entry mechanisms in primary human bronchial epithelial cells in vitro. H1N1pdm infection rapidly initiated a robust inflammatory gene signature (3 h post-infection) not elicited by sH1N1 infection. Protein secretion inhibition had no effect on gene induction. Infection with membrane fusion deficient H1N1pdm failed to induce robust inflammatory gene expression which was rescued with restoration of fusion ability, suggesting H1N1pdm directly triggered the inflammatory signature downstream of membrane fusion. Investigation of intra-virion components revealed H1N1pdm viral RNA (vRNA) triggered a stronger inflammatory phenotype than sH1N1 vRNA. Thus, our study is first to report H1N1pdm induces greater inflammatory gene expression than sH1N1 in vitro due to direct virus-epithelial cell interaction. Total RNA obtained from Normal Human Bronchial Epithelial Cells (NHBEC) at 3 hours or 24 hours post-infection with either 0.9 MOI A/Mexico/4108/2009 (H1N1) or 0.9 MOI A/Brisbane/59/2007 (H1N1). Total RNA was also collected at 0 hours from uninfected NHBEC for each infection. Changes in gene expression relative to uninfected cells were then investigated.

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