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

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.