Key result
ZVAD boosts EV-A71-infected cell viability by ~30 percentage points via ROS pathway regulation.
Why the study?
To evaluate the mechanism by which the caspase inhibitor ZVAD inhibits EV-A71 virus and provide an experimental basis for new antiviral drugs.
Absolute Event Rate: 83.7% vs 53.56%
ZVAD inhibits EV-A71 virus-induced apoptosis and inflammation in Vero cells via ROS-mediated signaling pathways, suggesting potential as an antiviral strategy.
May inform antiviral candidate selection for EV-A71; leaves open in vivo efficacy and clinical translation.
Emerging evidence that Enterovirus A 71 (EV-A71) infection closely related to apoptosis. The ZVAD is a caspase inhibitor that can prevent apoptosis. The aims of this project were to evaluate the mechanism of the ZVAD inhibited EV-A71 virus and to provide experiment basis for finding new antiviral drugs. In this study, after treated with ZVAD in EV-A71 infected Vero cells, the viral replication was reduced, and the cell viability was higher than EV-A71 group. Additionally, ZVAD decreased the cell apoptosis and the level of inflammatory cytokines induced by EV-A71 in the infected Vero cells. ZVAD inhibited cell apoptosis by regulating ROS mediated signaling pathway and inflammation cytokines to achieve antiviral.
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Xu et al. (2021) studied Enterovirus A71 (EV-A71) infection. ZVAD (zVAD-fmk) vs. EV-A71 infected Vero cells without ZVAD treatment was evaluated on Cell viability. ZVAD treatment of EV-A71 infected Vero cells increased cell viability from 53.56% to 83.7% and reduced apoptosis from 60.8% to 25.69% by regulating ROS mediated signaling pathways.
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