Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Comparative transcriptome analysis reveals key epigenetic targets in SARS-CoV-2 infection MESHD

    Authors: Marisol Salgado-Albarran; Erick I. Navarro-Delgado; Aylin Del Moral-Morales; Nicolas Alcaraz; Jan Baumbach; Rodrigo Gonzalez-Barrios; Ernesto Soto-Reyes

    id:2011.08902v1 Date: 2020-11-17 Source: arXiv

    COVID-19 MESHD is an infection caused by SARS-CoV-2 (Severe Acute Respiratory Syndrome coronavirus 2 MESHD), which has caused a global outbreak. Current research efforts are focused on the understanding of the molecular mechanisms involved in SARS-CoV-2 infection MESHD in order to propose drug-based therapeutic options. Transcriptional changes due to epigenetic regulation are key host cell responses to viral infection MESHD and have been studied in SARS-CoV and MERS-CoV; however, such changes are not fully described for SARS-CoV-2. In this study, we analyzed multiple transcriptomes obtained from cell lines infected with MERS-CoV, SARS-CoV and SARS-CoV-2 MESHD, and from COVID-19 MESHD patient-derived samples. Using integrative analyses of gene co-expression networks and de-novo pathway enrichment, we characterize different gene modules and protein pathways enriched with Transcription Factors or Epifactors relevant for SARS-CoV-2 infection MESHD. We identified EP300 HGNC, MOV10 HGNC, RELA HGNC and TRIM25 HGNC as top candidates, and more than 60 additional proteins involved in the epigenetic response during viral infection that have therapeutic potential. Our results show that targeting the epigenetic machinery could be a feasible alternative to treat COVID-19 MESHD.

    The Zinc Finger Antiviral Protein restricts SARS-CoV-2

    Authors: Rayhane Nchioua; Janis Mueller; Carina Conzelmann; Ruediger Gross; Steffen Stenger; Daniel Sauter; Jan Muench; Konstantin MJ Sparrer; Frank Kirchhoff

    doi:10.1101/2020.06.04.134379 Date: 2020-06-04 Source: bioRxiv

    Recent evidence shows that the Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) is highly sensitive to interferons (IFNs). However, the underlying antiviral effectors remain to be defined. Here, we show that Zinc finger antiviral protein ( ZAP HGNC) that specifically targets CpG dinucleotides in viral RNA sequences restricts SARS-CoV-2. We demonstrate that ZAP HGNC and its cofactors KHNYN HGNC and TRIM25 HGNC are expressed in human lung cells. Type I, II and III IFNs all strongly inhibited SARS-CoV-2 and further induced ZAP HGNC expression. Strikingly, SARS-CoV-2 and its closest relatives from bats show the strongest CpG suppression among all known human and bat coronaviruses, respectively. Nevertheless, knock-down of ZAP HGNC significantly increased SARS-CoV-2 production in lung cells, particularly upon treatment with IFN- HGNC or IFN-{gamma HGNC}. Thus, our results identify ZAP HGNC as an effector of the IFN response against SARS-CoV-2, although this pandemic pathogen may be preadapted to the low CpG environment in humans. HighlightsO_LISARS-CoV-2 and its closest bat relatives show strong CpG suppression C_LIO_LIIFN-{beta}, -{gamma} and -{lambda} inhibit SARS-CoV-2 with high efficiency C_LIO_LIZAP restricts SARS-CoV-2 and contributes to the antiviral effect of IFNs C_LI

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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