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10.1016/j.molcel.2021.04.008

http://scihub22266oqcxt.onion/10.1016/j.molcel.2021.04.008

33930332!8043580!33930332
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      Mol+Cell 2021 ; 81 (12): 2656-2668.e8
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Functional landscape of SARS-CoV-2 cellular restriction JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=33930332 #FOAvip A deficient interferon (IFN) response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated as a determinant of severe coronavirus disease 2019 (COVID-19). To identify the molecular effectors that govern IFN control of SARS-CoV-2 infection, we conducted a large-scale gain-of-function analysis that evaluated the impact of human IFN-stimulated genes (ISGs) on viral replication. A limited subset of ISGs were found to control viral infection, including endosomal factors inhibiting viral entry, RNA binding proteins suppressing viral RNA synthesis, and a highly enriched cluster of endoplasmic reticulum (ER)/Golgi-resident ISGs inhibiting viral assembly/egress. These included broad-acting antiviral ISGs and eight ISGs that specifically inhibited SARS-CoV-2 and SARS-CoV-1 replication. Among the broad-acting ISGs was BST2/tetherin, which impeded viral release and is antagonized by SARS-CoV-2 Orf7a protein. Overall, these data illuminate a set of ISGs that underlie innate immune control of SARS-CoV-2/SARS-CoV-1 infection, which will facilitate the understanding of host determinants that impact disease severity and offer potential therapeutic strategies for COVID-19.
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Functional landscape of SARS-CoV-2 cellular restriction ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=33930332 #FOAvip
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<ref>{{Cite pmid|33930332}}</ref>

Functional landscape of SARS-CoV-2 cellular restriction #MMPMID33930332
Martin-Sancho L; Lewinski MK; Pache L; Stoneham CA; Yin X; Becker ME; Pratt D; Churas C; Rosenthal SB; Liu S; Weston S; De Jesus PD; O'Neill AM; Gounder AP; Nguyen C; Pu Y; Curry HM; Oom AL; Miorin L; Rodriguez-Frandsen A; Zheng F; Wu C; Xiong Y; Urbanowski M; Shaw ML; Chang MW; Benner C; Hope TJ; Frieman MB; Garcia-Sastre A; Ideker T; Hultquist JF; Guatelli J; Chanda SK
Mol Cell 2021[Jun]; 81 (12): 2656-2668.e8 PMID33930332show ga
A deficient interferon (IFN) response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated as a determinant of severe coronavirus disease 2019 (COVID-19). To identify the molecular effectors that govern IFN control of SARS-CoV-2 infection, we conducted a large-scale gain-of-function analysis that evaluated the impact of human IFN-stimulated genes (ISGs) on viral replication. A limited subset of ISGs were found to control viral infection, including endosomal factors inhibiting viral entry, RNA binding proteins suppressing viral RNA synthesis, and a highly enriched cluster of endoplasmic reticulum (ER)/Golgi-resident ISGs inhibiting viral assembly/egress. These included broad-acting antiviral ISGs and eight ISGs that specifically inhibited SARS-CoV-2 and SARS-CoV-1 replication. Among the broad-acting ISGs was BST2/tetherin, which impeded viral release and is antagonized by SARS-CoV-2 Orf7a protein. Overall, these data illuminate a set of ISGs that underlie innate immune control of SARS-CoV-2/SARS-CoV-1 infection, which will facilitate the understanding of host determinants that impact disease severity and offer potential therapeutic strategies for COVID-19.
|Animals[MESH]
|Antigens, CD/chemistry/*genetics/immunology[MESH]
|Binding Sites[MESH]
|Cell Line, Tumor[MESH]
|Chlorocebus aethiops[MESH]
|Endoplasmic Reticulum/genetics/immunology/virology[MESH]
|GPI-Linked Proteins/chemistry/genetics/immunology[MESH]
|Gene Expression Regulation[MESH]
|Golgi Apparatus/genetics/immunology/virology[MESH]
|HEK293 Cells[MESH]
|Host-Pathogen Interactions/*genetics/immunology[MESH]
|Humans[MESH]
|Immunity, Innate[MESH]
|Interferon Regulatory Factors/classification/*genetics/immunology[MESH]
|Interferon Type I/*genetics/immunology[MESH]
|Molecular Docking Simulation[MESH]
|Protein Binding[MESH]
|Protein Conformation, alpha-Helical[MESH]
|Protein Conformation, beta-Strand[MESH]
|Protein Interaction Domains and Motifs[MESH]
|SARS-CoV-2/*genetics/immunology[MESH]
|Signal Transduction[MESH]
|Vero Cells[MESH]
|Viral Proteins/chemistry/*genetics/immunology[MESH]
|Virus Internalization[MESH]
|Virus Release/genetics/immunology[MESH]Functional landscape of SARS-CoV-2 cellular restriction (epmc).pdf

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