Lei Ma,1 Yanyan Wang,1 Ying Liu,2 Jinshen Wang,1 Yueqin Han,1 Daogang Qin,1 Han Yan3 

1Department of Pediatrics, Liaocheng People’s Hospital, Liaocheng, People’s Republic of China; 2Department of Medical, Liaocheng People’s Hospital, Liaocheng, People’s Republic of China; 3Shandong Provincial Key Laboratory for Pediatrics of Integrated Traditional and Western Medicine, Liaocheng People’s Hospital, Liaocheng, People’s Republic of China

Correspondence: Han Yan, Shandong Provincial Key Laboratory for Pediatrics of Integrated Traditional and Western Medicine, Liaocheng People’s Hospital, No. 67 West Dongchang Road, Liaocheng, 252000, People’s Republic of China, Email yanhan186@163.com

Purpose: This study aimed to clarify the molecular mechanisms of Qingre Jiedu Decoction (QJD), a traditional Chinese medicine (TCM), in treating infectious mononucleosis (IM). By combining network pharmacology and clinical trial validation, the research sought to understand how QJD interacts with biological pathways to combat IM.
Methods: The research team identified active compounds and their targets in QJD using databases like TCMSP and STITCH. Genes related to IM were sourced from NCBI and DisGeNET. These data were used to construct a protein-protein interaction (PPI) network with STRING, visualizing interactions between QJD targets and IM-related genes. Functional enrichment analyses were conducted, including GO biological process analysis via Cytoscape ClueGo and KEGG pathway analysis using R’s Clusterprofile package. A clinical trial involving 97 pediatric IM patients (53 in the experimental group, 44 in the control group) evaluated QJD’s real-world efficacy.
Results: The study identified 156 active compounds and 401 targets in QJD, along with 15 potential therapeutic targets for IM. In the clinical trial, the experimental group showed a significantly higher negative rate of plasma EBV (Epstein-Barr virus)-DNA post-treatment, indicating a stronger antiviral effect. Peripheral blood lymphocyte counts, CD3+ percentage, and CD8+ percentage decreased in the experimental group, suggesting an immunomodulatory effect. Additionally, levels of inflammatory cytokines (IL-6, IL-1β, TNF-α) were significantly reduced post-treatment, supporting QJD’s anti-inflammatory properties.
Conclusion: QJD’s multi-component effects contribute to its antiviral activity against EBV by modulating cytokine-mediated signaling pathways. This finding provides a scientific basis for QJD’s clinical use in IM and underscores the potential of integrating network pharmacology with clinical trials to elucidate TCM mechanisms.

Keywords: QJD, IM, EBV, network pharmacology, clinical efficacy, children