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SARS-CoV-2 proteins

NSP3 (1)


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    Novel Mutations in NSP1 HGNC and PLPro of SARS-CoV-2 NIB-1 Genome Mount for Effective Therapeutics

    Authors: Mohammad Uzzal Hossain; Arittra Bhattacharjee; Md. Tabassum Hossain Emon; Zeshan Mahmud Chowdhury; Md. Golam Mosaib; Md. Moniruzzaman; Md. Hadisur Rahman; Md. Nazrul Islam; Irfan Ahmed; Md. Ruhul Amin; Asif Rashed; Keshob Chandra Das; Chaman Ara Keya; Md. Salimullah; Maria Elvira Balcells; Luis Rojas; Bruno Nervi; Jyh Kae Nien; Javier Garate; Carolina Prieto; Sofia Palma; Carolina Escobar; Josefina bascunan; Rodrigo Munoz; Monica Pinto; Daniela Cardemil; Marcelo Navarrete; Soledad Reyes; Victoria Espinoza; Nicolas Yanez; Christian Caglevic

    doi:10.1101/2020.12.02.408229 Date: 2020-12-02 Source: bioRxiv

    Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2), the etiologic agent of Coronavirus Disease MESHD- 2019 ( COVID-19 MESHD), is rapidly accumulating new mutations. Analysis of these mutations is necessary for gaining knowledge regarding different aspects of therapeutic development. Recently, we have reported a Sanger method based genome sequence of a viral isolate named SARS-CoV-2 NIB-1, circulating in Bangladesh. The genome has four novel mutations in V121D, V843F, A889V and G1691C positions. V121D substitution has the potential to destabilize the Non-Structural Protein ( NSP-1 HGNC) which inactivates the type-1 Interferon-induced antiviral system hence this mutant could be the basis of attenuated vaccines against SARS-CoV-2. V843F, A889V and G1691C are all located in NSP3 PROTEIN NSP3 HGNC. G1691C can decrease the flexibility of the protein while V843F and A889V changed the binding pattern of SARS-CoV-2 Papain MESHD Papain-Like protease PROTEIN (PLPro) inhibitor GRL0617. V843F PLPro showed reduced affinity for Interferon Stimulating Gene-15 ( ISG-15 HGNC) protein whereas V843F+A889V double mutants exhibited the same binding affinity as wild type PLPro. Here, V843F is a conserved position of PLPro that damaged the structure but A889V, a less conserved residue, most probably neutralized that damage. Mutants of NSP1 HGNC could provide attenuated vaccines against coronavirus. Also, these mutations of PLPro could be targeted to develop anti-SARS therapeutics.

    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.

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