Abstract
The susceptibility of ten EV-68 isolates (belonging to cluster A, B and C) to (entero-)virus inhibitors with different mechanisms of action was investigated. 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 a weak inhibitor. Resistance to pleconaril maps to V69A in VP1 and resistance to rupintrivir to V104I in the 3C protease. A structural explanation is provided why both mutations may cause resistance.
Original language | English |
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Pages (from-to) | 7782-7785 |
Journal | Antimicrobial Agents and Chemotherapy |
Volume | 59 |
Issue number | 12 |
DOIs | |
Publication status | Published - 14 Sept 2015 |