Why the study?
Does suramin reduce mortality and viral load in preclinical models of EV71 infection?
Does suramin reduce mortality and viral load in preclinical models of EV71 infection?
Suramin inhibits EV71 infection in vitro and in vivo, identifying it as a potential clinical candidate for EV71 treatment.
Suramin shows promise against EV71 in animals; leaves open whether efficacy translates to human trials.
Enterovirus 71 (EV71) causes severe central nervous system infections, leading to cardiopulmonary complications and death in young children. There is an urgent unmet medical need for new pharmaceutical agents to control EV71 infections. Using a multidisciplinary approach, we found that the approved pediatric antiparasitic drug suramin blocked EV71 infectivity by a novel mechanism of action that involves binding of the naphtalentrisulonic acid group of suramin to the viral capsid. Moreover, we demonstrate that when suramin is used in vivo at doses equivalent to or lower than the highest dose already used in humans, it significantly decreased mortality in mice challenged with a lethal dose of EV71 and peak viral load in adult rhesus monkeys. Thus, suramin inhibits EV71 infection by neutralizing virus particles prior to cell attachment. Consequently, these findings identify suramin as a clinical candidate for further development as a therapeutic or prophylactic treatment for severe EV71 infection.
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Ren et al. (2014) studied this question.
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