Evolution-Driven Attenuation of Alphaviruses Highlights Key Glycoprotein Determinants Regulating Viral Infectivity and Dissemination.
E1 glycoprotein
alphaviruses
chikungunya virus
cholesterol dependence
fusion
viral dissemination
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
09 07 2019
09 07 2019
Historique:
received:
17
12
2018
revised:
08
05
2019
accepted:
05
06
2019
entrez:
11
7
2019
pubmed:
11
7
2019
medline:
29
9
2020
Statut:
ppublish
Résumé
Understanding the fundamental mechanisms of arbovirus transmission and pathogenesis is essential to develop strategies for treatment and prevention. We previously took an in vivo evolution-based approach and identified the chikungunya virus E1 glycoprotein residue 80 to play a critical role in viral transmission and pathogenesis. In this study, we address the genetic conservation and function of position 80 and demonstrate that this residue is a key determinant in alphavirus infectivity and dissemination through modulation of viral fusion and cholesterol dependence. In addition, in studying the evolution of position 80, we identified a network of glycoprotein residues, including epidemic determinants, that regulate virus dissemination and infectivity. These studies underscore the importance of taking evolution-based approaches to not only identify key viral determinants driving arbovirus transmission and pathogenesis but also to uncover fundamental aspects of arbovirus biology.
Identifiants
pubmed: 31291581
pii: S2211-1247(19)30788-0
doi: 10.1016/j.celrep.2019.06.022
pmc: PMC7141928
mid: NIHMS1575554
pii:
doi:
Substances chimiques
Glycoproteins
0
Viral Envelope Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
460-471.e5Subventions
Organisme : NIAID NIH HHS
ID : T32 AI007180
Pays : United States
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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