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ORIGINAL RESEARCH article

Front. Vet. Sci.
Sec. Veterinary Infectious Diseases
Volume 12 - 2025 | doi: 10.3389/fvets.2025.1524812

Exploring the Antiviral Potential of Shikimic Acid against Chikungunya Virus through Network Pharmacology, Molecular Docking, and In Vitro Experiments

Provisionally accepted
  • 1 Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China
  • 2 College of Animal Science and Technology, Guangxi University, Nanning, Guangxi Zhuang Region, China
  • 3 Institute of Virology, Wenzhou University, Wenzhou, Zhejiang Province, China
  • 4 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, Hebei Province, China

The final, formatted version of the article will be published soon.

    Chikungunya virus (CHIKV) is an arbovirus that can lead to chronic arthritis and significantly diminish the quality of life of patients. Given the expanding global prevalence of CHIKV and the absence of specific antiviral therapies, there is an urgent need to explore effective treatment options .This study aimed to evaluate the antiviral effects of shikimic acid (SA) against CHIKV through a combination of network pharmacology, molecular docking, and in vitro assays. Network pharmacology analysis identified 26 potential targets through which SA could inhibit CHIKV, including key pathogenic targets such as TNF, IL-6, and MAPK3. This hypothesis was further supported by molecular docking. The molecular docking analysis revealed that SA could interact with multiple CHIKV-related targets, including EGF, with vina scores generally lower than -6, indicating a high propensity for stable complex formation. The results also suggested that SA could potentially disrupt the IL-17 signaling pathway by engaging with various targets to form complexes.In vitro experiments confirmed that SA significantly enhanced the viability of 293T and BHK-21 cells infected with CHIKV by approximately 25% and reduced viral load by over 20% at concentrations ranging from 1000 μM to 31.25 μM. Additionally, SA was found to markedly downregulate the expression of CHIKV-related attachment factors ACTG1, TSPAN9, and TIM-1 in 293T cells infected with CHIKV. Furthermore, RT-qPCR analysis demonstrated that SA effectively decreased the expression of NFKB1, PTGS2, RELA, and EGF related to the IL-17 signaling pathway. In conclusion, these findings indicate that SA is a promising candidate for developing treatment strategies targeting CHIKV with good clinical application value.

    Keywords: CHIKV, Shikimic Acid, antiviral, Network Pharmacology, molecular docking

    Received: 08 Nov 2024; Accepted: 07 Jan 2025.

    Copyright: © 2025 Xin, Song, Zheng, Li, Qin, Wang, Zhang and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Wei Wang, Institute of Virology, Wenzhou University, Wenzhou, Zhejiang Province, China
    He Zhang, Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, Hebei Province, China
    Guangneng Peng, Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.