Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68

Liang Sun; Adam Meijer; Mathy Froeyen; Linlin Zhang; Hendrik Jan Thibaut; Jim Baggen; Shyla George; John Vernachio; Frank J.M. Van Kuppeveld; Pieter Leyssen; Rolf Hilgenfeld; Johan Neyts; Leen Delang

doi:10.1128/AAC.01375-15

Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68

Liang Sun, Adam Meijer, Mathy Froeyen, Linlin Zhang, Hendrik Jan Thibaut, Jim Baggen, Shyla George, John Vernachio, Frank J.M. Van Kuppeveld, Pieter Leyssen, Rolf Hilgenfeld, Johan Neyts^*, Leen Delang

^*Corresponding author for this work

72 Citations (Scopus)

Abstract

We 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.

Original language	English
Journal	Antimicrobial Agents and Chemotherapy
Volume	59
Issue number	12
Pages (from-to)	7782-7785
Number of pages	4
ISSN	0066-4804
DOIs	https://doi.org/10.1128/AAC.01375-15
Publication status	Published - 01.12.2015

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Sun, L., Meijer, A., Froeyen, M., Zhang, L., Thibaut, H. J., Baggen, J., George, S., Vernachio, J., Van Kuppeveld, F. J. M., Leyssen, P., Hilgenfeld, R., Neyts, J., & Delang, L. (2015). Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68. Antimicrobial Agents and Chemotherapy, 59(12), 7782-7785. https://doi.org/10.1128/AAC.01375-15

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abstract = "We 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.",

author = "Liang Sun and Adam Meijer and Mathy Froeyen and Linlin Zhang and Thibaut, \{Hendrik Jan\} and Jim Baggen and Shyla George and John Vernachio and \{Van Kuppeveld\}, \{Frank J.M.\} and Pieter Leyssen and Rolf Hilgenfeld and Johan Neyts and Leen Delang",

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Sun, L, Meijer, A, Froeyen, M, Zhang, L, Thibaut, HJ, Baggen, J, George, S, Vernachio, J, Van Kuppeveld, FJM, Leyssen, P, Hilgenfeld, R, Neyts, J & Delang, L 2015, 'Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68', Antimicrobial Agents and Chemotherapy, vol. 59, no. 12, pp. 7782-7785. https://doi.org/10.1128/AAC.01375-15

TY - JOUR

T1 - Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68

AU - Sun, Liang

AU - Meijer, Adam

AU - Froeyen, Mathy

AU - Zhang, Linlin

AU - Thibaut, Hendrik Jan

AU - Baggen, Jim

AU - George, Shyla

AU - Vernachio, John

AU - Van Kuppeveld, Frank J.M.

AU - Leyssen, Pieter

AU - Hilgenfeld, Rolf

AU - Neyts, Johan

AU - Delang, Leen

PY - 2015/12/1

Y1 - 2015/12/1

N2 - We 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.

AB - We 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.

UR - https://www.scopus.com/pages/publications/84948126432

U2 - 10.1128/AAC.01375-15

DO - 10.1128/AAC.01375-15

M3 - Journal articles

C2 - 26369972

AN - SCOPUS:84948126432

SN - 0066-4804

VL - 59

SP - 7782

EP - 7785

JO - Antimicrobial Agents and Chemotherapy

JF - Antimicrobial Agents and Chemotherapy

IS - 12

ER -

Antiviral activity of broad-spectrum and enterovirus-specific inhibitors against clinical isolates of enterovirus D68

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