ArticleJournal of virology2025
Classical swine fever virus utilizes stearoyl-CoA desaturase 1-mediated lipid metabolism to facilitate viral replication.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Japanese encephalitis virus orchestrates GLUT4-mediated glucose metabolism to potentiate viral replication via insulin receptor signaling.PLoS pathogens · 2026Article
- Review
- The implications of FASN in viral infection and related diseases: a promising target in antiviral therapies.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Viral infections can significantly alter cellular lipid metabolism by modulating key rate-limiting enzymes, including fatty acid synthase (FASN), stearoyl-CoA desaturase 1 (SCD1), and acetyl-CoA carboxylase (ACC). Our previous study revealed the pivotal role of FASN in lipid droplet (LD) synthesis and the promotion of classical swine fever virus (CSFV) replication. However, the roles of the other two key enzymes in CSFV infection remain unexplored. In this study, we screened a library of 96 lipid metabolism-targeted compounds and identified an antiviral inhibitor of SCD1, a rate-limiting enzyme in monounsaturated fatty acid synthesis, that inhibits CSFV replication. Suppressing SCD1 activity through inhibitors or small interfering RNA knockdown reduces CSFV proliferation. However, this suppression is reversed by adding SCD1 active products (oleic acid/palmitoleic acid [OA/PA]), highlighting the essential role of SCD1 in CSFV proliferation. Mechanistically, CSFV non-structural protein p7 interacts with SCD1 and recruits it to the viral replication complex (VRC) during infection. Importantly, CSFV infection activates the endoplasmic reticulum stress pathway IRE1α/XBP1, which positively regulates SCD1 expression, leading to increased production of triglyceride (TG) and LDs and subsequently enhancing CSFV replication. In summary, our study elucidates the critical role of SCD1 in the CSFV life cycle and highlights its potential as an antiviral target for developing new therapies against
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Registered trials
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