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Transcriptomic profiling and genomic mutational analysis of Human coronavirus (HCoV)-229E -infected human cells

Friedman, Nehemya ; Jacob-Hirsch, Jasmine ; Drori, Yaron ; Eran, Eyal ; Kol, Nitzan ; Nayshool, Omri ; Mendelson, Ella ; Rechavi, Gideon ; Mandelboim, Michal Kumar, Binod

PloS one, 2021-02, Vol.16 (2), p.e0247128-e0247128 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Transcriptomic profiling and genomic mutational analysis of Human coronavirus (HCoV)-229E -infected human cells
Autor: Friedman, Nehemya ; Jacob-Hirsch, Jasmine ; Drori, Yaron ; Eran, Eyal ; Kol, Nitzan ; Nayshool, Omri ; Mendelson, Ella ; Rechavi, Gideon ; Mandelboim, Michal
Kumar, Binod
Assuntos: Analysis ; Biological response modifiers ; Biology and Life Sciences ; Biosynthesis ; BRCA1 protein ; Cancer ; Cell cycle ; Cell Line ; Cholesterol ; Coronaviridae ; Coronavirus 229E, Human - physiology ; Coronavirus Infections - genetics ; Coronaviruses ; Deoxyribonucleic acid ; DNA ; DNA biosynthesis ; DNA damage ; Double-stranded RNA ; eIF-2 kinase ; Elongation ; Epidemiology ; Gene expression ; Gene sequencing ; Genetic aspects ; Genomic analysis ; Health care facilities ; High-Throughput Nucleotide Sequencing ; Host-Pathogen Interactions ; Humans ; Infections ; Initiation factor eIF-2 ; Interferon ; Kinases ; Medical research ; Medicine ; Medicine and Health Sciences ; Methodology ; Middle East respiratory syndrome ; Next-generation sequencing ; Preventive medicine ; Protein kinase ; Public health ; Research facilities ; Respiratory diseases ; Ribonucleic acid ; RNA ; RNA viruses ; Transcriptome ; Transcriptomics ; Translation ; Translation elongation ; Translation initiation ; Viruses
É parte de: PloS one, 2021-02, Vol.16 (2), p.e0247128-e0247128
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Competing Interests: The authors have declared that no competing interests exist.
Descrição: 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 MRC-5 cells showed marked downregulation of superpathway of cholesterol biosynthesis and eIF2 signaling pathways. Moreover, upregulation of cyclins, cell cycle control of chromosomal replication, and the role of BRCA1 in DNA damage response, alongside downregulation of the cell cycle G1/S checkpoint, suggest that HCoV-229E may favors S phase for viral infection. Intriguingly, a significant portion 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. On the other hand, early upregulation of the antiviral response factor Apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B) was observed. APOBEC3B cytidine deaminase signature (C-to-T) was previously observed in genomic analysis of SARS-CoV-2 but not HCoV-229E. Higher levels of C-to-T mutations were found in countries with high mortality rates caused by SARS-CoV-2. APOBEC activity could be a marker for new emerging CoVs. This study will enhance our understanding of commonly circulating HCoVs and hopefully provide critical information about still-emerging coronaviruses.
Editor: United States: Public Library of Science
Idioma: Inglês

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Transcriptomic profiling and genomic mutational analysis of Human coronavirus (HCoV)-229E -infected human cells

Friedman, Nehemya ; Jacob-Hirsch, Jasmine ; Drori, Yaron ; Eran, Eyal ; Kol, Nitzan ; Nayshool, Omri ; Mendelson, Ella ; Rechavi, Gideon ; Mandelboim, Michal Kumar, Binod

United States: Public Library of Science

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