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Article: High-throughput identification of loss-of-function mutations for anti-interferon activity in the influenza a virus ns segment

TitleHigh-throughput identification of loss-of-function mutations for anti-interferon activity in the influenza a virus ns segment
Authors
Issue Date2014
Citation
Journal of Virology, 2014, v. 88, n. 17, p. 10157-10164 How to Cite?
Abstract© 2014, American Society for Microbiology. All Rights Reserved. Viral proteins often display several functions which require multiple assays to dissect their genetic basis. Here, we describe a systematic approach to screen for loss-of-function mutations that confer a fitness disadvantage under a specified growth condition. Our methodology was achieved by genetically monitoring a mutant library under two growth conditions, with and without interferon, by deep sequencing. We employed a molecular tagging technique to distinguish true mutations from sequencing error. This approach enabled us to identify mutations that were negatively selected against, in addition to those that were positively selected for. Using this technique, we identified loss-of-function mutations in the influenza A virus NS segment that were sensitive to type I interferon in a high-throughput fashion. Mechanistic characterization further showed that a single substitution, D92Y, resulted in the inability of NS to inhibit RIG-I ubiquitination. The approach described in this study can be applied under any specified condition for any virus that can be genetically manipulated.
Persistent Identifierhttp://hdl.handle.net/10722/285752
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, Nicholas C.-
dc.contributor.authorYoung, Arthur P.-
dc.contributor.authorAl-Mawsawi, Laith Q.-
dc.contributor.authorAnders Olson, C.-
dc.contributor.authorFeng, Jun-
dc.contributor.authorQi, Hangfei-
dc.contributor.authorLuan, Harding H.-
dc.contributor.authorLi, Xinmin-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:33Z-
dc.date.available2020-08-18T04:56:33Z-
dc.date.issued2014-
dc.identifier.citationJournal of Virology, 2014, v. 88, n. 17, p. 10157-10164-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285752-
dc.description.abstract© 2014, American Society for Microbiology. All Rights Reserved. Viral proteins often display several functions which require multiple assays to dissect their genetic basis. Here, we describe a systematic approach to screen for loss-of-function mutations that confer a fitness disadvantage under a specified growth condition. Our methodology was achieved by genetically monitoring a mutant library under two growth conditions, with and without interferon, by deep sequencing. We employed a molecular tagging technique to distinguish true mutations from sequencing error. This approach enabled us to identify mutations that were negatively selected against, in addition to those that were positively selected for. Using this technique, we identified loss-of-function mutations in the influenza A virus NS segment that were sensitive to type I interferon in a high-throughput fashion. Mechanistic characterization further showed that a single substitution, D92Y, resulted in the inability of NS to inhibit RIG-I ubiquitination. The approach described in this study can be applied under any specified condition for any virus that can be genetically manipulated.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleHigh-throughput identification of loss-of-function mutations for anti-interferon activity in the influenza a virus ns segment-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.01494-14-
dc.identifier.pmid24965464-
dc.identifier.pmcidPMC4136320-
dc.identifier.scopuseid_2-s2.0-84910670272-
dc.identifier.volume88-
dc.identifier.issue17-
dc.identifier.spage10157-
dc.identifier.epage10164-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000341232300055-
dc.identifier.issnl0022-538X-

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