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Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication
Xiuwen Yang1, Jiayi Chen1, Zixin Lu1
1BSL-3 Laboratory, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Frontiers in Microbiology
|October 17, 2022
Summary
Enterovirus A71 (EV-A71) replication is primarily impacted by lipid metabolism, not endoplasmic reticulum (ER) stress. Targeting lipid beta-oxidation offers a promising strategy for controlling EV-A71 infections and hand-foot-and-mouth disease (HFMD).
Area of Science:
- Virology
- Molecular Biology
- Pathogenesis
Background:
- Enterovirus A71 (EV-A71) causes severe hand-foot-and-mouth disease (HFMD) in children.
- Pathogenic mechanisms of EV-A71, particularly lipid metabolism and ER stress, are not fully understood.
- Viral infections often involve alterations in host lipid homeostasis and endoplasmic reticulum (ER) stress.
Purpose of the Study:
- To investigate the roles of lipid metabolism and ER stress in EV-A71 replication.
- To identify potential antiviral targets by characterizing EV-A71-induced metabolic and stress responses.
- To determine whether lipid metabolism or ER stress is the primary driver of EV-A71 replication.
Main Methods:
- Utilized chemical inhibitors (PKR IN, Tunicamycin, TOFA, C75, Etomoxir) and activators (oleic acid) to modulate ER stress and lipid metabolism.
- Assessed the impact of these modulations on EV-A71 replication.
- Measured changes in lipid levels and ER stress markers post-infection and treatment.
Main Results:
- Inhibiting ER stress reduced EV-A71 replication and lipid levels.
- Inhibiting fatty acid synthesis (TOFA, C75) decreased viral replication.
- Enhancing triacylglycerol (oleic acid) or inhibiting carnitine palmitoyltransferase 1 (Etomoxir) also reduced EV-A71 replication.
- Lipid beta-oxidation was identified as a key factor influencing EV-A71 replication, while ER stress appeared to be a secondary, non-restrictive change.
Conclusions:
- Lipid metabolism, specifically beta-oxidation, plays a crucial role in EV-A71 replication.
- ER stress is a concomitant change during EV-A71 infection but does not appear to restrict viral replication.
- Targeting lipid metabolic pathways, particularly beta-oxidation, presents a potential therapeutic strategy against EV-A71.
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