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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    Type-I interferon signatures in SARS-CoV-2 infected MESHD Huh7 cells


    doi:10.1101/2021.02.04.429738 Date: 2021-02-04 Source: bioRxiv

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) that causes Coronavirus disease 2019 MESHD ( COVID-19 MESHD) has caused a global health emergency. A key feature of COVID-19 MESHD is dysregulated interferon-response. Type-I interferon (IFN-I) is one of the earliest antiviral innate immune responses following viral infection MESHD and plays a significant role in the pathogenesis of SARS-CoV-2. In this study, using a proteomics-based approach, we identified that SARS-CoV-2 infection MESHD induces delayed and dysregulated IFN-I MESHD signaling in Huh7 cells. We demonstrate that SARS-CoV-2 is able to inhibit RIG-I mediated IFN-b production. Our results also confirm the recent findings that IFN-I pretreatment is able to reduce susceptibility of Huh7 cells to SARS-CoV-2, but not post-treatment. Moreover, senescent Huh7 cells, in spite of showing accentuated IFN-I response were more susceptible to SARS-CoV-2 infection MESHD, and the virus effectively inhibited IFIT1 HGNC in these cells. Finally, proteomic comparison between SARS-CoV-2, SARS-CoV and MERS-CoV revealed a distinct differential regulatory signature of interferon-related proteins emphasizing that therapeutic strategies based on observations in SARS-CoV and MERS-CoV should be used with caution. Our findings provide a better understanding of SARS-CoV-2 regulation of cellular interferon response and a perspective on its use as a treatment. Investigation of different interferon stimulated genes and their role in inhibition of SARS-CoV-2 pathogenesis may direct novel antiviral strategies.

    Early temporal dynamics of cellular responses to SARS-CoV-2

    Authors: Arinjay Banerjee; Patrick Budylowski; Daniel Richard; Hassaan Maan; Jennifer Aguiar; Nader El-Sayes; Benjamin J.-M. Tremblay; Sam Afkhami; Mehran Karimzadeh; Lily Yip; Mario A Ostrowski; Jeremy A Hirota; Robert Kozak; Terence D Capellini; Matthew S. Miller; Andrew G McArthur; Bo Wang; Andrew C Doxey; Samira Mubareka; Karen Mossman

    doi:10.1101/2020.06.18.158154 Date: 2020-06-18 Source: bioRxiv

    Two highly pathogenic human coronaviruses that cause severe acute respiratory syndrome MESHD (SARS) and Middle East respiratory syndrome MESHD ( MERS MESHD) have evolved proteins that can inhibit host antiviral responses, likely contributing to disease progression and high case-fatality rates. SARS-CoV-2 emerged in December 2019 resulting in a global pandemic. Recent studies have shown that SARS-CoV-2 is unable to induce a robust type I interferon (IFN) HGNC response in human cells, leading to speculation about the ability of SARS-CoV-2 to inhibit innate antiviral responses. However, innate antiviral responses are dynamic in nature and gene expression levels rapidly change within minutes to hours. In this study, we have performed a time series RNA-seq and selective immunoblot analysis of SARS-CoV-2 infected lung MESHD (Calu-3) cells to characterize early virus-host processes. SARS-CoV-2 infection MESHD upregulated transcripts for type I IFNs and interferon stimulated genes (ISGs) after 12 hours. Furthermore, we analyzed the ability of SARS-CoV-2 to inhibit type I IFN production and downstream antiviral signaling in human cells. Using exogenous stimuli, we discovered that SARS-CoV-2 is unable to modulate IFN{beta HGNC} production and downstream expression of ISGs, such as IRF7 HGNC and IFIT1 HGNC. Thus, data from our study indicate that SARS-CoV-2 may have evolved additional mechanisms, such as masking of viral nucleic acid sensing by host cells to mount a dampened innate antiviral response. Further studies are required to fully identify the range of immune-modulatory strategies of SARS-CoV-2. SignificanceHighly pathogenic coronaviruses that cause SARS and MERS have evolved proteins to shutdown antiviral responses. The emergence and rapid spread of SARS-CoV-2, along with its relatively low case-fatality rate have led to speculation about its ability to modulate antiviral responses. We show that SARS-CoV-2 is unable to block antiviral responses that are mounted by exogenous stimuli. Data from our study provide promising support for the use of recombinant type I IFN as combination therapy to treat COVID-19 MESHD patients. Furthermore, our data also suggest that the inability of SARS-CoV-2 to efficiently modulate antiviral responses may be associated with its low case-fatality rate compared to other pathogenic CoVs that cause SARS and MERS.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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