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Single-cell studies of IFN-β promoter activation by wildtype and NS1-defective influenza A viruses

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Date
03/2017
Author
Killip, Marian Jane
Jackson, David
Pérez - Cidoncha, Maite
Fofor, Ervin
Randall, Richard Edward
Funder
The Wellcome Trust
Grant ID
101788/Z/13/Z
Keywords
Influenza virus
NS1
Interferon
IFN
Innate immune response
Interferon antagonist
QR180 Immunology
QR355 Virology
RB Pathology
NDAS
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Abstract
Deletion or truncation of NS1, the principal interferon (IFN) antagonist of influenza viruses, leads to increased IFN induction during influenza virus infection. We have studied activation of the IFN induction cascade by both wildtype and NS1-defective viruses at the single-cell level using a cell line expressing GFP under the control of the IFN-β promoter and by examining MxA expression. The IFN-β promoter was not activated in all infected cells, even during NS1-defective virus infections. Loss of NS1 expression is therefore by itself insufficient to induce IFN in an infected cell, and factors besides NS1 expression status must dictate whether the IFN response is activated. The IFN response was efficiently stimulated in these cells following infection with other viruses; the differential IFN response we observe with influenza viruses is therefore not cell-specific, but is likely due to differences in the nature of the infecting virus particles and their subsequent replication.
Citation
Killip , M J , Jackson , D , Pérez - Cidoncha , M , Fofor , E & Randall , R E 2017 , ' Single-cell studies of IFN-β promoter activation by wildtype and NS1-defective influenza A viruses ' , Journal of General Virology , vol. 98 , no. 3 , pp. 357-363 . https://doi.org/10.1099/jgv.0.000687
Publication
Journal of General Virology
Status
Peer reviewed
DOI
https://doi.org/10.1099/jgv.0.000687
ISSN
0022-1317
Type
Journal article
Rights
Copyright 2017 The Authors. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
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  • University of St Andrews Research
URI
http://hdl.handle.net/10023/10527

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