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Discovering antiviral restriction factors and pathways using genetic screens

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Jones_2021_JGV_Antiviral_CC.pdf (1.537Mb)
Date
21/05/2021
Author
Jones, Chloe E.
Tan, Wenfang Spring
Grey, Finn
Hughes, David John
Keywords
Innate immunity
CRISPR–Cas9
Genome-wide screens
RNAi
Antiviral immunity
Interferon
QR355 Virology
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Abstract
Viral infections activate the powerful interferon (IFN) response that induces the expression of several hundred IFN stimulated genes (ISGs). The principal role of this extensive response is to create an unfavourable environment for virus replication and to limit spread; however, untangling the biological consequences of this large response is complicated. In addition to a seemingly high degree of redundancy, several ISGs are usually required in combination to limit infection as individual ISGs often have low to moderate antiviral activity. Furthermore, what ISG or combination of ISGs are antiviral for a given virus is usually not known. For these reasons, and that the function(s) of many ISGs remains unexplored, genome-wide approaches are well placed to investigate what aspects of this response results in an appropriate, virus-specific phenotype. This review discusses the advances screening approaches have provided for the study of host defence mechanisms, including CRISPR/Cas9, ISG expression libraries and RNAi technologies.
Citation
Jones , C E , Tan , W S , Grey , F & Hughes , D J 2021 , ' Discovering antiviral restriction factors and pathways using genetic screens ' , Journal of General Virology , vol. 102 , no. 5 , 0001603 . https://doi.org/10.1099/jgv.0.001603
Publication
Journal of General Virology
Status
Peer reviewed
DOI
https://doi.org/10.1099/jgv.0.001603
ISSN
0022-1317
Type
Journal item
Rights
Copyright © 2021 The Authors. This is an Open Access article published by the Microbiology Society under the Creative Commons Attribution License.
Description
Research in the Hughes lab is supported by a grant from the Academy of Medical Sciences (SFB003/1028), a grant from Tenovus Scotland (T20/63), and The Wellcome Trust Institutional Strategic Support Fund (ISSF). Research in the Gray lab is supported Medical Research Council (MR/N001796/1) and the Biotechnology and Biological Sciences Research Council (BBS/E/D/20002172). C. E. J. is supported by a University of St Andrews Ph.D. scholarship.
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  • University of St Andrews Research
URI
http://hdl.handle.net/10023/23279

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