Key result
Luteolin inhibited EV71 and CA16 viral infection with an EC50 of approximately 10 μM by targeting the post-attachment stage of viral RNA replication.
Luteolin demonstrates potent in vitro antiviral activity against EV71 and CA16 by inhibiting viral RNA replication, suggesting potential as a lead compound for drug development.
Luteolin merits exploration as an enterovirus inhibitor; leaves open clinical applicability pending further studies.
Hand, foot and mouth disease (HFMD) is a common pediatric illness mainly caused by infection with enterovirus 71 (EV71) and coxsackievirus A16 (CA16). The frequent HFMD outbreaks have become a serious public health problem. Currently, no vaccine or antiviral drug for EV71/CA16 infections has been approved. In this study, a two-step screening platform consisting of reporter virus-based assays and cell viability‑based assays was developed to identify potential inhibitors of EV71/CA16 infection. Two types of reporter viruses, a pseudovirus containing luciferase-encoding RNA replicons encapsidated by viral capsid proteins and a full-length reporter virus containing enhanced green fluorescent protein, were used for primary screening of 400 highly purified natural compounds. Thereafter, a cell viability-based secondary screen was performed for the identified hits to confirm their antiviral activities. Three compounds (luteolin, galangin, and quercetin) were identified, among which luteolin exhibited the most potent inhibition of viral infection. In the cell viability assay and plaque reduction assay, luteolin showed similar 50% effective concentration (EC50) values of about 10 μM. Luteolin targeted the post-attachment stage of EV71 and CA16 infection by inhibiting viral RNA replication. This study suggests that luteolin may serve as a lead compound to develop potent anti-EV71 and CA16 drugs.
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Xu et al. (2014) studied Hand, foot and mouth disease (EV71 and CA16 infection). Luteolin was evaluated on Inhibition of viral infection (50% effective concentration) (EC50 ~10 μM). Luteolin inhibited EV71 and CA16 viral infection with an EC50 of approximately 10 μM by targeting the post-attachment stage of viral RNA replication.
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