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Transcriptomic profiling of human corona virus (HCoV)-229E -infected human cells

ABSTRACT: Transcriptomic profiling of human corona virus (HCoV)-229E -infected human cells

PROVIDER: PRJNA656274 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12424243.fastq.gz	Fastqsanger.gz
	SRR12424244.fastq.gz	Fastqsanger.gz
	SRR12424245.fastq.gz	Fastqsanger.gz
	SRR12424246.fastq.gz	Fastqsanger.gz
	SRR12424247.fastq.gz	Fastqsanger.gz

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Transcriptomic profiling of human corona virus (HCoV)-229E -infected human cells

Project description:Human coronaviruses (HCoVs) cause mild to severe respiratory infection. Most of the common cold illnesses are caused by one of four HCoVs, namely HCoV-229E, HCoV-NL63, HCoV-HKU1 and HCoV-OC43. Several studies have applied global transcriptomic methods to understand host responses to HCoV infection, with most studies focusing on the pandemic severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome CoV (MERS-CoV) and the newly emerging SARS-CoV-2. In this study, Next Generation Sequencing was used to gain new insights into cellular transcriptomic changes elicited by alphacoronavirus HCoV-229E. HCoV-229E-infected MRC5 cells showed marked downregulation of superpathway of cholesterol biosynthesis and eIF2 signaling pathways. Moreover, upregulation of cyclins, cell cycle control of chromosomal replication, and role of BRCA1 in DNA damage response, alongside downregulation of the cell cycle G1/S checkpoint, suggest that HCoV-229E favors S phase for viral infection. Intriguingly, more than 80% of key factors of cell innate immunity, interferon-stimulated genes (ISGs) and other transcripts of early antiviral response genes were downregulated early in HCoV-229E infection. This study will enhance our understanding of commonly circulating HCoVs and hopefully provide critical information about still-emerging coronaviruses.

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