ArticleVirology journal2025
Inhibitory effect of Alantolactone against varicella-zoster virus in vitro.
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Alantolactone inhibits T-cell lymphoma progression by suppressing CD47 expression via the PI3K/AKT and ERK signaling pathways.Apoptosis : an international journal on programmed cell death · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundVaricella-zoster virus (VZV), a member of the α-herpesvirus family, is known for causing two distinct diseases: chickenpox (varicella) during the primary infection and shingles (zoster) due to reactivation of the virus later in life. Although there are vaccines available to prevent VZV infection, it is still not universally effective, and antiviral treatments for VZV are limited and may come with significant side effects. Thus, development of novel therapeutics is urgently needed.
methodsWe identified a naturally occurring Alantolactone (ALT) that inhibited replication of recombinant VZV in human diploid fibroblast (WI-38 cells) and Adult Retinal Pigment Epithelial cell line-19 (ARPE-19 cells) through Western blotting, qPCR and plaque assays. Subsequently, we explored the mechanism underlying the anti-VZV activity of ALT using time-of-addition experiments and transcriptomic analyses.
resultsA screening model was established for anti-VZV compounds, and we screened ALT was with good anti-VZV efficacy. Our findings revealed that ALT alleviated cytopathic changes, reduced viral titres, and inhibited the expression of viral genes and proteins in WI-38 cells and ARPE-19 cells. Furthermore, our data showed that ALT inhibited VZV infection in intracellular viral replication. Finally, multiple inflammatory pathways were involved in the antiviral role of ALT, and IL-6 was one of the most critical hub genes.
conclusionTogether, our findings identify ALT as an anti-VZV agent that may prove useful in the treatment of VZV replication.
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