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ChIP-seq analysis of coronavirus-infected human cells

ABSTRACT: The aim of the experiment is to identify chromatin and transcription factor binding dynamics in host gene expression upon infection of human Huh7 hepatoma carcinoma cells with human coronavirus HCoV-229E as compared to uninfected cells and in comparison to cells stimulated by IL-1alpha (10ng/ml) for 1h. All experiments have been performed at 33°C which is required for sufficient viral entry/replication.

ORGANISM(S): Homo sapiens

PROVIDER: GSE89212 | GEO | 2017/03/15

SECONDARY ACCESSION(S): PRJNA350685

REPOSITORIES: GEO

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HCoV-229E infection of the human HuH7 cell line [Experiment B]

Project description:The aim of the experiment is to identify changes in host gene expression upon infection of Huh7 hepatoma carcinoma cells with human coronavirus HCoV-229E as compared to uninfected cells and in comparison to cells stimulated by IL-1alpha (10ng/ml) for 1h. All experiments have been performed at 33°C which is required for sufficient viral entry/replication. Also included are two samples which have been treated with a heat inactivated coronavirus (56°C for 5min).

2017-03-15 | GSE89166 | GEO

Time-course of HCoV-229E infection of A549 cells

Project description:The aim of the experiment is to identify kinetic changes in host gene expression upon infection of A549 lung epithelial carcinoma cells with human corona virus HCoV-229E as compared to unifected cells. Negativ controls include infections with heat-inactivated virus. Positive controls include treatment of cells with human IL-1alpha (10ng/ml) for 1h. All experiments have been performed at 33°C which is required for sufficient viral entry/replication.

2017-03-15 | GSE89159 | GEO

HCoV-229E infection of the human HuH7 cell line [Experiment A]

Project description:The aim of the experiment is to identify changes in host gene expression upon infection of HuH7 human hepatoma cells with Human corona virus-229E (HCoV-229E) compared to mock-infected cells. All experiments were performed at 33°C which is required for sufficient viral entry/replication.

2017-03-15 | GSE89160 | GEO

p97/VCP as a therapy target for developing drugs against human coronavirus

Project description:Understanding how human coronavirus dysregulate host proteome during infection in human cells will identify general pathways that are common to coronavirus infection. NMS-873 is an allosteric p97/VCP ATPase inhibitor and was show to have antiviral effect in multiple viruses including SARS-CoV2. We first demonstrated that genetic knock down of p97 reduced HCoV-229E, HCoV-OC43 infection and secretion. To investigate how p97/VCP assists virus infection, we used unbiased quantitative proteomics to compare dysregulated proteomes caused by HCoV-229E, HCoV-OC43 and SARS-CoV2 infection. We then compared dysregulated proteomes after HCoV-229E and HCoV-OC43 infection with and without p97 knockdown. Moreover, we elucidated the impact of p97 on different stages of viral life cycle using two potent p97 inhibitors, CB-5083 and NMS-873 and demonstrate their can block HCoV replication. Together, our data provide insights to repurpose potential cancer drugs that target the essential host protein p97/VCP.

2021-11-03 | PXD026216 | Pride

Functional interrogation of a SARS-CoV-2 host protein interactome identifies unique and shared coronavirus host factors

Project description:The ongoing SARS-CoV-2 pandemic has devastated the global economy and claimed more than one million lives, presenting an urgent global health crisis. To identify host factors required for infection by SARS-CoV-2 and seasonal coronaviruses, we designed a focused high-coverage CRISPR-Cas9 library targeting 332 members of a recently published SARS-CoV-2 protein interactome. We leveraged the compact nature of this library to systematically screen SARS-CoV-2 at two physiologically relevant temperatures (33 ºC and 37 ºC) along with three related coronaviruses (HCoV-229E, HCoV-NL63, and HCoV-OC43), allowing us to probe this interactome at a much higher resolution relative to genome scale studies. This approach yielded several new insights, including unexpected virus-specific differences in Rab GTPase requirements and GPI anchor biosynthesis, as well as identification of multiple pan-coronavirus factors involved in cholesterol homeostasis. This coronavirus essentiality catalog could inform ongoing drug development efforts aimed at intercepting and treating COVID-19, and help prepare for future coronavirus outbreaks.

2020-11-24 | GSE162039 | GEO

Cell host-response to infection with novel human coronavirus EMC predict potential antivirals and important differences with SARS-coronavirus.

Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection. Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected. Samples were collected 0, 3, 7, 12, 18 and 24 hpi. There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check). There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi. For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).

2013-05-03 | E-GEOD-45042 | biostudies-arrayexpress

ZBTB7A promotes virus-host homeostasis during human coronavirus 229E infection II

Project description:In this study, we define ZBTB7A as a driver of cellular survival during HCoV-229E infection.

2022-10-05 | GSE197882 | GEO

ZBTB7A promotes virus-host homeostasis during human coronavirus 229E infection I

Project description:In this study, we define ZBTB7A as a driver of cellular survival during HCoV-229E infection.

2022-10-05 | GSE197644 | GEO

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.

2021-03-03 | GSE155986 | GEO

Genome-scale identification of SARS-CoV-2 and pan-coronavirus host factor networks

Project description:The COVID-19 pandemic has claimed the lives of more than one million people worldwide. The causative agent, SARS-CoV-2, is a member of the Coronaviridae family, which are viruses that cause respiratory infections of varying severity. The cellular host factors and pathways co-opted by SARS- CoV-2 and other coronaviruses in the execution of their life cycles remain ill-defined. To develop an extensive compendium of host factors required for infection by SARS-CoV-2 and three seasonal coronaviruses (HCoV-OC43, HCoV-NL63, and HCoV-229E), we performed parallel genome-scale CRISPR knockout screens. These screens uncovered multiple host factors and pathways with pan- coronavirus and virus-specific functional roles, including major dependency on glycosaminoglycan biosynthesis, SREBP signaling, BMP signaling, and glycosylphosphatidylinositol biosynthesis, as well as a requirement for several poorly characterized proteins. We identified an absolute requirement for the VTT-domain containing protein TMEM41B for infection by SARS-CoV-2 and three seasonal coronaviruses. This human Coronaviridae host factor compendium represents a rich resource to develop new therapeutic strategies for acute COVID-19 and potential future coronavirus spillover events.

2020-11-24 | GSE162038 | GEO

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