A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion

Plants pre-infected with a mild variant of a virus frequently become protected against more severe variants of the same virus through the cross protection phenomenon first discovered in 1929. Despite its widespread use in managing important plant virus diseases, the mechanism of cross protection rem...

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Main Authors: Xiao-Feng Zhang, Shaoyan Zhang, Qin Guo, Rong Sun, Taiyun Wei, Feng Qu
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-01-01
Series:Frontiers in Plant Science
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fpls.2018.00040/full
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author Xiao-Feng Zhang
Shaoyan Zhang
Qin Guo
Rong Sun
Taiyun Wei
Feng Qu
author_facet Xiao-Feng Zhang
Shaoyan Zhang
Qin Guo
Rong Sun
Taiyun Wei
Feng Qu
author_sort Xiao-Feng Zhang
collection DOAJ
description Plants pre-infected with a mild variant of a virus frequently become protected against more severe variants of the same virus through the cross protection phenomenon first discovered in 1929. Despite its widespread use in managing important plant virus diseases, the mechanism of cross protection remains poorly understood. Recent investigations in our labs, by analyzing the whole-plant dynamics of a turnip crinkle virus (TCV) population, coupled with cell biological interrogation of individual TCV variants, revealed possible novel mechanisms for cross protection and the closely related process of superinfection exclusion (SIE). Our new mechanistic model postulates that, for RNA viruses like TCV, SIE manifests a viral function that denies progeny viruses the chance of re-replicating their genomes in the cells of their “parents,” and it collaterally targets highly homologous superinfecting viruses that are indistinguishable from progeny viruses. We further propose that SIE may be evolutionarily selected to maintain an optimal error frequency in progeny genomes. Although primarily based on observations made with TCV, this new model could be broadly applicable to other viruses as it provides a molecular basis for maintaining virus genome fidelity in the face of the error-prone nature of virus replication process.
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spelling doaj.art-75ddb6750b35417993e026d897aa8e342022-12-21T18:39:32ZengFrontiers Media S.A.Frontiers in Plant Science1664-462X2018-01-01910.3389/fpls.2018.00040319005A New Mechanistic Model for Viral Cross Protection and Superinfection ExclusionXiao-Feng Zhang0Shaoyan Zhang1Qin Guo2Rong Sun3Taiyun Wei4Feng Qu5State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, Fujian Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, ChinaDepartment of Plant Pathology, Ohio Agricultural Research and Development Center, Ohio State University, Wooster, OH, United StatesDepartment of Plant Pathology, Ohio Agricultural Research and Development Center, Ohio State University, Wooster, OH, United StatesDepartment of Plant Pathology, Ohio Agricultural Research and Development Center, Ohio State University, Wooster, OH, United StatesState Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, Fujian Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, ChinaDepartment of Plant Pathology, Ohio Agricultural Research and Development Center, Ohio State University, Wooster, OH, United StatesPlants pre-infected with a mild variant of a virus frequently become protected against more severe variants of the same virus through the cross protection phenomenon first discovered in 1929. Despite its widespread use in managing important plant virus diseases, the mechanism of cross protection remains poorly understood. Recent investigations in our labs, by analyzing the whole-plant dynamics of a turnip crinkle virus (TCV) population, coupled with cell biological interrogation of individual TCV variants, revealed possible novel mechanisms for cross protection and the closely related process of superinfection exclusion (SIE). Our new mechanistic model postulates that, for RNA viruses like TCV, SIE manifests a viral function that denies progeny viruses the chance of re-replicating their genomes in the cells of their “parents,” and it collaterally targets highly homologous superinfecting viruses that are indistinguishable from progeny viruses. We further propose that SIE may be evolutionarily selected to maintain an optimal error frequency in progeny genomes. Although primarily based on observations made with TCV, this new model could be broadly applicable to other viruses as it provides a molecular basis for maintaining virus genome fidelity in the face of the error-prone nature of virus replication process.http://journal.frontiersin.org/article/10.3389/fpls.2018.00040/fullcross protectionsuperinfection exclusionturnip crinkle virusp28protein polymerization
spellingShingle Xiao-Feng Zhang
Shaoyan Zhang
Qin Guo
Rong Sun
Taiyun Wei
Feng Qu
A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
Frontiers in Plant Science
cross protection
superinfection exclusion
turnip crinkle virus
p28
protein polymerization
title A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
title_full A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
title_fullStr A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
title_full_unstemmed A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
title_short A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion
title_sort new mechanistic model for viral cross protection and superinfection exclusion
topic cross protection
superinfection exclusion
turnip crinkle virus
p28
protein polymerization
url http://journal.frontiersin.org/article/10.3389/fpls.2018.00040/full
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