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Open AccessArticle

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

by Yu-Wen Liao 1, Bing-Ching Ho 2, Min-Hsuan Chen 2 and Sung-Liang Yu 1,2,3,4,5,6,*
1
Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
2
Centers of Genomic and Precision Medicine, National Taiwan University, Taipei 100, Taiwan
3
Department of Laboratory Medicine, National Taiwan University Hospital, Taipei 100, Taiwan
4
Institute of Medical Device and Imaging, College of Medicine, National Taiwan University, Taipei 100, Taiwan
5
Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
6
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei 100, Taiwan
*
Author to whom correspondence should be addressed.
Pathogens 2020, 9(2), 121; https://doi.org/10.3390/pathogens9020121
Received: 15 January 2020 / Revised: 3 February 2020 / Accepted: 11 February 2020 / Published: 14 February 2020
(This article belongs to the Section Human Pathogens)
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.
Keywords: Enterovirus 71; TCRβ repertoires; VP1; CDR3; pathogenesis Enterovirus 71; TCRβ repertoires; VP1; CDR3; pathogenesis
MDPI and ACS Style

Liao, Y.-W.; Ho, B.-C.; Chen, M.-H.; Yu, S.-L. Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster. Pathogens 2020, 9, 121.

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