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Updated: Aug 4, 2025
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Targeting HDAC11 activity by FT895 restricts EV71 replication.
Hong Xie1, Enhui Yang2, Chaoyong Wang3
1Department of Gynecology Nursing, West China Second University Hospital, Sichuan University/West China School of Nursing, Sichuan University, Chengdu, Sichuan, China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, Sichuan, China.
Histone deacetylase 11 (HDAC11) supports Enterovirus 71 (EV71) replication, the cause of hand, foot, and mouth disease (HFMD). Targeting HDAC11 with an inhibitor (FT895) effectively restricted EV71, offering a potential new treatment for HFMD.
Area of Science:
- Virology
- Epigenetics
- Drug Discovery
Background:
- Enterovirus 71 (EV71) causes hand, foot, and mouth disease (HFMD), a significant pediatric health concern.
- Current treatments for HFMD lack specificity, highlighting the need for novel therapeutic targets and drugs.
Purpose of the Study:
- To investigate the role of histone deacetylase 11 (HDAC11) in EV71 replication.
- To evaluate the therapeutic potential of targeting HDAC11 against EV71 infection.
Main Methods:
- Utilized HDAC11 siRNA to downregulate HDAC11 expression.
- Administered the HDAC11 inhibitor FT895.
- Assessed EV71 replication in vitro and in vivo.
Main Results:
- HDAC11 was found to be involved in supporting EV71 replication.
- Downregulation of HDAC11 expression significantly restricted EV71 replication.
- FT895 demonstrated efficacy as an EV71 inhibitor in both in vitro and in vivo models.
Conclusions:
- HDAC11 plays a crucial role in the replication cycle of EV71.
- Targeting HDAC11 represents a promising therapeutic strategy for HFMD.
- FT895 is identified as a potential drug candidate for treating EV71 infections.
