Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster

Enterovirus 71 (EV71) has become an important public health problem in the Asia-Pacific region in the past decades. EV71 infection might cause neurological and psychiatric complications and even death. Although an EV71 vaccine has been currently approved, there is no effective therapy for treating E...

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Main Authors: Yu-Wen Liao, Bing-Ching Ho, Min-Hsuan Chen, Sung-Liang Yu
Format: Article
Language:English
Published: MDPI AG 2020-02-01
Series:Pathogens
Subjects:
Online Access:https://www.mdpi.com/2076-0817/9/2/121
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author Yu-Wen Liao
Bing-Ching Ho
Min-Hsuan Chen
Sung-Liang Yu
author_facet Yu-Wen Liao
Bing-Ching Ho
Min-Hsuan Chen
Sung-Liang Yu
author_sort Yu-Wen Liao
collection DOAJ
description Enterovirus 71 (EV71) has become an important public health problem in the Asia-Pacific region in the past decades. EV71 infection might cause neurological and psychiatric complications and even death. Although an EV71 vaccine has been currently approved, there is no effective therapy for treating EV71-infected patients. Virus infections have been reported to shape host T cell receptor (TCR) repertoire. Therefore, understanding of host TCR repertoire in EV71 infection could better the knowledge in viral pathogenesis and further benefit the anti-viral therapy development. In this study, we used a mouse-adapted EV71 (mEV71) model to observe changes of host TCR repertoire in an EV71-infected central nervous system. Neonate mice were infected with mEV71 and mouse brainstem TCRβ repertoires were explored. Here, we reported that mEV71 infection impacted host brainstem TCRβ repertoire, where mEV71 infection skewed TCRβ diversity, changed VJ combination usages, and further expanded specific TCRβ CDR3 clones. Using bioinformatics analysis and ligand-binding prediction, we speculated the expanded TCRβ CDR3 clone harboring CASSLGANSDYTF sequence was capable of binding cleaved EV71 VP1 peptides in concert with major histocompatibility complex (MHC) molecules. We observed that mEV71 infection shaped host TCRβ repertoire and presumably expanded VP1-specific TCRβ CDR3 in mEV71-infected mouse brainstem that integrated EV71 pathogenesis in central nervous system.
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spelling doaj.art-50fe62d1c6d741e99dac778ab77125fe2022-12-22T04:28:30ZengMDPI AGPathogens2076-08172020-02-019212110.3390/pathogens9020121pathogens9020121Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 ClusterYu-Wen Liao0Bing-Ching Ho1Min-Hsuan Chen2Sung-Liang Yu3Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei 100, TaiwanCenters of Genomic and Precision Medicine, National Taiwan University, Taipei 100, TaiwanCenters of Genomic and Precision Medicine, National Taiwan University, Taipei 100, TaiwanDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei 100, TaiwanEnterovirus 71 (EV71) has become an important public health problem in the Asia-Pacific region in the past decades. EV71 infection might cause neurological and psychiatric complications and even death. Although an EV71 vaccine has been currently approved, there is no effective therapy for treating EV71-infected patients. Virus infections have been reported to shape host T cell receptor (TCR) repertoire. Therefore, understanding of host TCR repertoire in EV71 infection could better the knowledge in viral pathogenesis and further benefit the anti-viral therapy development. In this study, we used a mouse-adapted EV71 (mEV71) model to observe changes of host TCR repertoire in an EV71-infected central nervous system. Neonate mice were infected with mEV71 and mouse brainstem TCRβ repertoires were explored. Here, we reported that mEV71 infection impacted host brainstem TCRβ repertoire, where mEV71 infection skewed TCRβ diversity, changed VJ combination usages, and further expanded specific TCRβ CDR3 clones. Using bioinformatics analysis and ligand-binding prediction, we speculated the expanded TCRβ CDR3 clone harboring CASSLGANSDYTF sequence was capable of binding cleaved EV71 VP1 peptides in concert with major histocompatibility complex (MHC) molecules. We observed that mEV71 infection shaped host TCRβ repertoire and presumably expanded VP1-specific TCRβ CDR3 in mEV71-infected mouse brainstem that integrated EV71 pathogenesis in central nervous system.https://www.mdpi.com/2076-0817/9/2/121enterovirus 71tcrβ repertoiresvp1cdr3pathogenesis
spellingShingle Yu-Wen Liao
Bing-Ching Ho
Min-Hsuan Chen
Sung-Liang Yu
Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
Pathogens
enterovirus 71
tcrβ repertoires
vp1
cdr3
pathogenesis
title Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
title_full Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
title_fullStr Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
title_full_unstemmed Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
title_short Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster
title_sort enterovirus 71 infection shapes host t cell receptor repertoire and presumably expands vp1 specific tcrβ cdr3 cluster
topic enterovirus 71
tcrβ repertoires
vp1
cdr3
pathogenesis
url https://www.mdpi.com/2076-0817/9/2/121
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