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Published on: July 17, 2019
RASSF4 promotes EV71 replication to accelerate the inhibition of the phosphorylation of AKT
Fengfeng Zhang1, Yongjuan Liu2, Xiong Chen3
1Pathogenic Organism and Infectious Diseases Research Institute, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Hubei Province Key Laboratory of Allergy and Immunology, Wuhan 430071, China.
Abstract:
Enterovirus 71 (EV71) is a neurotropic virus that causes hand, foot and mouth disease (HFMD), occasionally leading to death. As a member of the RAS association domain family (RASSFs), RASSF4 plays important roles in cell death, tumor development and signal transduction. However, little is known about the relationship between RASSF4 and EV71. Our study reveals for the first time that RASSF4 promotes EV71 replication and then accelerates AKT phosphorylation inhibition in EV71-infected 293T cells, suggesting that RASSF4 may be a potential new target for designing therapeutic measures to prevent and control EV71 infection.
Insights
This study shows that RASSF4 protein enhances Enterovirus 71 (EV71) replication and inhibits AKT phosphorylation. RASSF4 emerges as a potential therapeutic target for controlling EV71 infections and hand, foot, and mouth disease (HFMD).
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Enterovirus 71 (EV71) causes severe hand, foot, and mouth disease (HFMD), posing a significant public health threat.
- RASSF4, a member of the RAS association domain family, is implicated in cell death and tumor development.
- The interaction between EV71 and RASSF4 remains largely unexplored.
Purpose of the Study:
- To investigate the role of RASSF4 in EV71 infection.
- To elucidate the molecular mechanisms by which RASSF4 influences EV71 replication and host cell signaling.
Main Methods:
- EV71 infection of 293T cells.
- Analysis of RASSF4 expression and its impact on viral replication.
- Assessment of AKT phosphorylation levels in infected cells.
Main Results:
- RASSF4 was found to promote EV71 replication in infected cells.
- RASSF4 accelerated the inhibition of AKT phosphorylation following EV71 infection.
- This suggests a novel interaction influencing viral pathogenesis.
Conclusions:
- RASSF4 plays a significant role in supporting EV71 replication.
- RASSF4 modulates AKT signaling pathways during EV71 infection.
- RASSF4 represents a potential therapeutic target for managing EV71 infections.
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