ArticleJournal of virology2026
Lysophosphatidic acid promotes lipid metabolism through AMPK signaling to support Coxsackievirus infection.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Lysophosphatidic acid (LPA) is a bioactive signaling lipid that regulates cellular processes, including growth, survival, differentiation, and metabolic homeostasis. LPA signals through its G-protein-coupled receptor, LPA receptor 1 (LPAR1), to modulate pathways controlling cellular signaling and metabolism. Viruses rely on cellular metabolism for efficient replication, and lipids function at nearly every stage in virus replication. Using Coxsackievirus B3 (CVB3) as a model, we performed global metabolomic analysis of infected Huh7 cells and identified lipid classes altered upon infection. Using small-molecule inhibitors targeting lipids, we identified LPA signaling as a key factor in CVB3 infection. Inhibiting LPA signaling with AM095 or via siRNA knockdown reduces CVB3 infection by over 100-fold. We find that LPA mediates CVB3 genome replication. Mechanistically, LPA signaling through LPAR1 facilitates cellular lipid synthesis by regulating AMPK and downstream enzymes, including fatty acid synthase (FASN) and acetyl-CoA carboxylase 1 (ACC1). In AM095-treated cells, lipid droplets are depleted, and cells exhibit a quiescent-like phenotype. Replenishing lipids fully rescues viral replication, indicating that LPA's proviral function is to facilitate lipid synthesis through AMPK signaling. These findings identify LPA-LPAR1 signaling as a regulator of host lipid metabolism that supports CVB3 replication, revealing a metabolic axis for antiviral intervention.IMPORTANCECellular metabolism supports virus infection by providing energy and the building blocks for virus replication. During viral infection, cellular metabolism changes drastically, and we find that lipids are among the most significantly changed metabolites during infection with Coxsackievirus B3, a picornavirus. We used metabolomics to characterize changes in metabolites in infected cells, and we followed up on these data with a drug screen with molecules targeting cellular lipid pathways. We identified lysophosphatidic acid (LPA) signaling as a major regulator of Coxsackievirus infection, supporting viral genome replication via lipid synthesis. This study underscores the importance of lipids in viral infection, uncovers new mechanisms by which LPA signals, and provides new insight into LPA's function in Coxsackievirus infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.