Author:
Sun Liang,Meijer Adam,Froeyen Mathy,Zhang Linlin,Thibaut Hendrik Jan,Baggen Jim,George Shyla,Vernachio John,van Kuppeveld Frank J. M.,Leyssen Pieter,Hilgenfeld Rolf,Neyts Johan,Delang Leen
Abstract
ABSTRACTWe investigated the susceptibility of 10 enterovirus D68 (EV-D68) isolates (belonging to clusters A, B, and C) to (entero)virus inhibitors with different mechanisms of action. The 3C-protease inhibitors proved to be more efficient than enviroxime and pleconaril, which in turn were more effective than vapendavir and pirodavir. Favipiravir proved to be a weak inhibitor. Resistance to pleconaril maps to V69A in the VP1 protein, and resistance to rupintrivir maps to V104I in the 3C protease. A structural explanation of why both substitutions may cause resistance is provided.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Pharmacology (medical),Pharmacology
Cited by
55 articles.
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