3C-protease inhibitors demonstrate superior in vitro efficacy against EV-D68 compared to other antivirals, with specific viral mutations identified that confer resistance.
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In vitro ranking of EV-D68 inhibitors supports prioritized preclinical testing; leaves open clinical efficacy and resistance dynamics.
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.
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Sun et al. (2015) studied this question.
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