Evaluation and mechanism study of Pien Tze Huang against EV-A71 infection

Hand, foot, and mouth disease (HFMD) caused by enterovirus A71 (EV-A71) infection, currently lacks specific preventive and therapeutic interventions. Here, we demonstrated that Pien Tze Huang (PZH) could dose-dependently inhibit EV-A71 replication at the cellular level, resulting in significant redu...

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Published inFrontiers in pharmacology Vol. 14; p. 1251731
Main Authors Wang, Huiqiang, Chen, Fenbei, Wang, Shicong, Li, Yuhuan, Liu, Ting, Li, Yinghong, Deng, Hongbin, Dong, Jingwen, Pang, Jing, Song, Danqing, Zhang, Dousheng, Yu, Juan, Wang, Yanxiang
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 26.10.2023
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Summary:Hand, foot, and mouth disease (HFMD) caused by enterovirus A71 (EV-A71) infection, currently lacks specific preventive and therapeutic interventions. Here, we demonstrated that Pien Tze Huang (PZH) could dose-dependently inhibit EV-A71 replication at the cellular level, resulting in significant reductions in EV-A71 virus protein 1 (VP1) expression and viral yields in Vero and human rhabdomyosarcoma cells. More importantly, we confirmed that PZH could protect mice from EV-A71 infection for the first time, with Ribavirin serving as a positive control. PZH treatment reduced EV-A71 VP1 protein expression, viral yields in infected muscles, and improved muscle pathology. Additionally, we conducted a preliminary mechanism study using quantitative proteomics. The results suggested that the suppression of the PI3K/AKT/mTOR and NF-κB signaling pathways may contribute to the anti-EV-A71 activity of PZH. These findings provide strong evidence supporting the potential therapeutic application of PZH for EV-A71 infection management.
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Edited by: Karunakaran Kalesh, Teesside University, United Kingdom
Reviewed by: Wei Ye, Air Force Medical University, China
Durbadal Ojha, National Institute of Allergy and Infectious Diseases (NIH), United States
These authors have contributed equally to this work and share first authorship
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2023.1251731