Our latest study (Glaziou et al., 2026, Mol Cell Life Sci) reveals that HEV hijacks host cell metabolism to fuel its replication:

• TCA cycle, mitochondrial oxidative phosphorylation (OXPHOS), fatty acid metabolism, and β-oxidation, are extensively rewired.
• Lipid storage organelles expand, long-chain neutral lipids accumulate, and pro-inflammatory oxylipins surge.
• HEV relies on lipid-fuelled OXPHOS rather than glycolysis.
• Distinct metabolic programs for HEV-1 versus HEV-3, aligning with their differential pathogenicity.

These findings highlight critical host metabolic vulnerabilities exploited by HEV and provide a roadmap for targeting metabolic hubs as therapy.

Interestingly, while our previous work in placental models (Gouilly et al., 2018, Nat Commun) showed HEV-1 triggers inflammatory damage at the maternal-fetal interface, the placenta is a highly active metabolic organ, and how HEV reshapes its metabolism remains an exciting question for future studies. 

Takeaway: HEV doesn’t just infect—it reprograms, fuels, and manipulates host metabolism to thrive. Understanding these strategies could point to novel therapeutic interventions.