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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    Association of Toll-like receptor 7 variants with life-threatening COVID-19 MESHD disease in males

    Authors: Chiara Fallerini; Sergio Daga; Stefania Mantovani; Elisa Benetti; Aurora Pujol; Nicola Picchiotti; Agatha Schluter; Laura Planas-Serra; Jesus Troya; Margherita Baldassarri; Francesca Fava; Serena Ludovisi; Francesco Castelli; Maria Eugenia Quiros-Roldan; Massimo Vaghi; Stefano Rusconi; Matteo Siano; Maria Bandini; Simone Furini; Francesca Mari; - GEN-COVID Multicenter Study; Alessandra Renieri; Mario U Mondelli; Elisa Frullanti

    doi:10.1101/2020.11.19.20234237 Date: 2020-11-27 Source: medRxiv

    Background: COVID-19 MESHD clinical presentation ranges from asymptomatic to fatal outcome. This variability is due in part to host genome specific mutations. Recently, two families in which COVID-19 MESHD segregates like an X-linked recessive monogenic disorder MESHD environmentally conditioned by SARS-CoV-2 have been reported leading to identification of loss-of-function variants in TLR7 HGNC. Objective: We sought to determine whether the two families represent the tip of the iceberg of a subset of COVID-19 MESHD male patients. Methods: We compared male subjects with extreme phenotype selected from the Italian GEN-COVID cohort of 1178 SARS-CoV-2-infected MESHD subjects (<60y, 79 severe cases versus 77 control cases). We applied the LASSO Logistic Regression analysis, considering only rare variants on the young male subset, picking up TLR7 HGNC as the most important susceptibility gene. Results: Rare TLR7 HGNC missense variants were predicted to impact on protein function in severely affected males and in none of the asymptomatic subjects. We then investigated a similar white European cohort in Spain, confirming the impact of TRL7 variants. A gene expression profile analysis in peripheral blood mononuclear cells after stimulation with TLR7 HGNC agonist demonstrated a reduction of mRNA level of TLR7 HGNC, IRF7 HGNC, ISG15 HGNC, IFN-[a] and IFN-{gamma HGNC} in COVID-19 MESHD patients compared with unaffected controls demonstrating an impairment in type I and II INF responses. Conclusion: Young males with TLR7 HGNC loss-of-function mutations and severe COVID-19 MESHD in the two reported families represent only a fraction of a broader and complex host genome situation. Specifically, missense mutations in the X-linked recessive TLR7 disorder MESHD TLR7 HGNC disorder may significantly contribute to disease susceptibility in up to 4% of severe COVID-19 MESHD.

    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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