ArticleViruses2025
Cinnamaldehyde Inhibits the Replication of Porcine Reproductive and Respiratory Syndrome Virus Type 2 In Vitro.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The roles and mechanisms of natural compounds in preventing and treating viral reproductive disorders in major economic livestock.Virulence · 2026Review
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Globally, the swine industry suffers significant economic losses due to the presence of porcine reproductive and respiratory syndrome virus (PRRSV). Unfortunately, existing vaccines fail to offer adequate protection against the various strains of PRRSV, and there are currently no specific treatments available for this virus. In this study, we screened four natural products and identified cinnamaldehyde (CA) as an effective inhibitor of PRRSV infection in Marc-145 cells. CA could achieve an inhibition rate of up to 93% on PRRSV N protein at 160 μM. Mechanistically, CA exerted anti-PRRSV ability in different treatment modes. CA could directly interact with PRRSV particles. Cinnamaldehyde blocks the binding, entry, replication, and release of PRRSV. Furthermore, a significant reduction in dsRNA levels was observed in the CA-treated groups compared to the control groups. In conclusion, our research demonstrated that CA could inhibit essential stages of the PRRSV lifecycle: binding, entry, replication, and release. CA could directly interact with PRRSV. Additionally, CA disrupted the expression of dsRNA during viral replication, thereby suppressing in vitro PRRSV replication in Marc-145 cells. This study provides crucial perspectives on the potential application of CA for the prevention and treatment of PRRS.
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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.