Pleconaril inhibits EV-D68 in vitro with a half maximal effective concentration (EC50) of 430 nM by binding to the viral capsid and preventing uncoating.
Targeting EV-D68, a respiratory virus A recent outbreak of respiratory illness in U.S. children was caused by entorovirus D68 (EV-D68). Enteroviruses also include human pathogens such as human rhinovirus, which causes the common cold, and poliovirus. Most of these viruses are stabilized by a factor that binds in a hydrophobic pocket of the capsid protein VP1, and antiviral compounds can act by displacing this factor. Liu et al. report the crystal structure of EV-D68 and its complex with the antiviral compound peconaril. In EV-D68, the hydrophobic pocket contained a fatty acid that was displaced by peconaril. Peconaril efficiently inhibited EV-D68 infection of cells, making it a possible drug candidate against EV-D68. Science , this issue p. 71
Liu et al. (Thu,) conducted a other in Enterovirus D68 (EV-D68) infection. Pleconaril vs. Pirodavir and BTA-188 was evaluated on Half maximal effective concentration (EC50). Pleconaril inhibits EV-D68 in vitro with a half maximal effective concentration (EC50) of 430 nM by binding to the viral capsid and preventing uncoating.
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