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. 2026 Sep 17;105(12):107795. doi: 10.1016/j.psj.2026.107795

Quercetin exhibits antiviral activity against duck Tembusu virus in vitro and in vivo

Jiawen Wang 1, Siqi Wang 1, Kuiru Fang 1, Yingying Yuan 1, Shinuo Fan 1, Qing Wang 1,⁎
PMCID: PMC13634505  PMID: 42785066

Abstract

Duck Tembusu virus (DTMUV) is an avian pathogenic flavivirus that causes substantial economic losses to the poultry industry in China and Southeast Asia. The current antiviral drugs for the prevention and treatment of DTMUV infection are limited. Quercetin is a natural flavonoid widely found in fruits and vegetables and has been reported to exhibit antiviral activity against many viruses. However, whether quercetin possesses antiviral activity against DTMUV remains unknown. Therefore, the present study aimed to investigate the antiviral efficacy of quercetin against DTMUV. A Cell Counting Kit-8 (CCK-8) assay was performed to evaluate the cytotoxicity of quercetin in BHK-21 cells. The antiviral activity of quercetin was assessed using 50% tissue culture infectious dose (TCID₅₀) assay, real-time quantitative PCR (RT–qPCR), Western blotting and indirect immunofluorescence assay (IFA). Molecular docking analysis was conducted to predict potential viral targets. Moreover, the antiviral efficacy of quercetin in vivo was further evaluated in DTMUV-infected goslings. The results of the CCK-8 assay revealed that quercetin at concentrations up to 40 μM had no significant effect on BHK-21 cells. Quercetin significantly inhibited DTMUV replication in BHK-21 cells in a dose- and time-dependent manner, as demonstrated by reduced viral titres, RNA copy numbers, and E protein expression. Direct virucidal assays revealed that quercetin could directly inactivate DTMUV particles. Adsorption and post-adsorption assays revealed that quercetin inhibited DTMUV infection during the post-adsorption stage. Furthermore, molecular docking predictions indicate that the viral NS5 protein is a potential target for quercetin. In vivo, quercetin treatment significantly improved the survival rate of infected goslings; reduced viral loads in the liver, spleen, and brain; and alleviated gross pathological lesions and histopathological damage caused by DTMUV infection. In conclusion, quercetin exhibits potent anti-DTMUV activity both in vitro and in vivo. These findings provide a theoretical basis for the development of quercetin as a natural antiviral agent and highlight its potential application in the prevention and control of DTMUV infection.

Keywords: Duck Tembusu virus, Quercetin, Antiviral activity, Viral replication, Gosling

Introduction

Duck Tembusu virus (DTMUV) is an emerging avian-origin virus belonging to the genus Orthoflavivirus within the family Flaviviridae (Cao et al., 2011; Wu et al., 2023). Since its outbreak in major duck-producing regions of China in 2010, it has caused severe economic losses to the poultry industry in China as well as in neighbouring countries such as Thailand and Malaysia (Cao et al., 2011; Tunterak et al., 2018; Zhang et al., 2020). DTMUV mainly infects waterfowl such as ducks and geese, causing severe decreases in egg production, growth retardation, neurological symptoms, and even death (Sun et al., 2014). DTMUV has a broad host range. In addition to infecting ducks and geese, it can also infect various avian species, including chickens, pigeons, sparrows, and penguins (Li et al., 2020; Chen et al., 2024). Under artificial conditions, DTMUV is capable of infecting mice (Pan et al., 2023), and reports have suggested its potential zoonotic risk (Pulmanausahakul et al., 2022). DTMUV has a strong transmission ability and can spread through mosquito vectors (Sanisuriwong et al., 2020), horizontal transmission (including direct contact and aerosol transmission) (Li et al., 2015), and vertical transmission (Zhang et al., 2015). Its broad host range and multiple transmission routes pose significant challenges to the prevention and control of DTMUV infection.

Currently, prevention and control strategies against DTMUV mainly include biosecurity management, mosquito control, and vaccination (Wu et al., 2023). Although commercially available inactivated and live attenuated DTMUV vaccines can reduce viral infection and transmission to a certain extent, the continuous viral evolution, limited cross-protection among different strains, and insufficient duration of immunity make it difficult for existing vaccines to completely control the spread of DTMUV (Wu et al., 2023; Xu et al., 2025). To date, relatively few reports on antiviral drugs against this virus have been published (Zhu et al., 2021; Cheng et al., 2024). Therefore, the development of effective anti-DTMUV agents is urgently needed. In recent years, several natural bioactive compounds, including lycorine (Lv et al., 2021), (-)-epigallocatechin-3-gallate (Zhu et al., 2021), and curcumin (Yin et al., 2025), have shown promising anti-DTMUV activity. Owing to their low toxicity, multitarget properties, and broad-spectrum antiviral activities, natural bioactive compounds are promising candidates for the development of novel antiviral agents.

Quercetin is a natural flavonoid bioactive compound widely found in fruits and vegetables and has attracted considerable attention because of its antioxidant, antiviral, antibacterial, and anti-inflammatory properties (Di Petrillo et al., 2022). In recent years, studies on the antiviral activity of quercetin have gradually increased, and quercetin has been reported to exhibit significant inhibitory effects against a variety of DNA and RNA viruses, such as herpes simplex virus 1 (HSV-1) (Yu et al., 2025), hepatitis B virus (Yang et al., 2026), influenza virus (Mehrbod et al., 2020), and dengue virus (Mukherjee and Tripathi, 2025). Its antiviral activity has been attributed to multiple mechanisms, including the inhibition of viral neuraminidase, proteases, and polymerases, as well as direct interactions with viral proteins (Di Petrillo et al., 2022; Carrillo-Martinez et al., 2024). In addition, quercetin interferes with viral attachment, entry, and replication while also modulating host immune responses (Di Petrillo et al., 2022; Nguyen and Bhattacharya, 2022). However, the antiviral activity of quercetin against DTMUV has not yet been explored, and the underlying mechanisms remain to be evaluated.

In this study, we investigated the inhibitory effect of quercetin on DTMUV replication in BHK-21 cells. Molecular docking analysis was subsequently performed to predict potential viral targets of quercetin. In addition, an animal experiment was performed to evaluate the preventive and therapeutic efficacy of quercetin against DTMUV infection in vivo. Collectively, our findings suggest that quercetin could serve as a promising candidate for the development of anti-DTMUV therapeutics.

Materials and methods

Virus, cells and drugs

The DTMUV strain AQ-19 (GenBank: MT708901.1) was isolated in 2019 from a young goose at a breeding farm in Anhui Province, China (Zhu et al., 2022). BHK-21 cells (ATCC: CCL-10) were cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) supplemented with 10% foetal bovine serum (FBS; Gibco, USA) at 37 °C in a humidified incubator containing 5% CO₂. Quercetin was purchased from Aladdin Biochemical Technology Co., Ltd. (Aladdin, Cat. No. Q111273, purity ≥ 98.5%, China), dissolved in dimethyl sulfoxide (DMSO; Solarbio, China), and stored at −80 °C until use.

Quercetin cytotoxicity assay

To exclude the potential effect of quercetin on BHK-21 cell viability, a Cell Counting Kit-8 (CCK-8; Beyotime, China) was used to evaluate the cytotoxicity of quercetin. BHK-21 cells were seeded in 96-well plates and cultured until they formed a confluent monolayer. The cells were then treated with quercetin at various concentrations (0, 5, 10, 20, 40, and 80 μM) and incubated at 37 °C in a humidified atmosphere containing 5% CO₂ for 48 h. After treatment, 10 μL of CCK-8 solution was added to each well, followed by further incubation for 2 h. Subsequently, the absorbance at 450 nm was measured using a microplate reader (Thermo, USA). Each condition was performed in quadruplicate wells and independently repeated three times.

In vitro antiviral activity of quercetin against DTMUV

BHK-21 cells were seeded in 12-well plates and cultured to 70–80% confluence. The cells were pretreated with different concentrations of quercetin (0, 5, 10, 20, and 40 μM) or DMSO as a control for 2 h. Subsequently, BHK-21 cells were washed 3 times with PBS and then infected with DTMUV AQ-19 at a multiplicity of infection (MOI) of 0.1 for 2 h. After viral adsorption, the inoculum was removed and replaced with low-serum DMEM containing 1% FBS and different concentrations of quercetin (0, 5, 10, 20, and 40 μM). Cells were further cultured for 48 h. Cell culture supernatants were collected for viral titration using a 50% tissue culture infectious dose (TCID₅₀) assay, while cell samples were harvested for determination of viral copy numbers by real-time quantitative PCR (RT‒qPCR) and detection of DTMUV E protein expression by Western blotting and indirect immunofluorescence assay (IFA).

In addition, BHK-21 cells were pretreated with 40 μM quercetin for 2 h and then washed with PBS before being infected with DTMUV AQ-19 at an MOI of 0.1 for 2 h. Then, the medium was replaced with low-serum DMEM containing 1% FBS and 40 μM quercetin. Cell samples were collected at 24, 36, and 48 h post-infection (hpi) for RT‒qPCR analysis of viral copy numbers and Western blot analysis of DTMUV E protein expression.

TCID₅₀ assay

Viral titres were determined via a TCID₅₀ assay as previously described (Zhou et al., 2023). BHK-21 cells were seeded in 96-well plates and cultured until they reached approximately 80% confluence. Afterwards, the cells were infected with a series of 1:10 dilutions of the virus sample, with eight wells per dilution. The plates were incubated at 37 °C in a humidified atmosphere containing 5% CO₂ for 72–96 h, and cytopathic effects were observed daily. The cytopathic lesions were recorded, and the TCID₅₀ was calculated using the Reed–Muench method.

RNA extraction and RT‒qPCR

Total RNA was extracted from BHK-21 cells or tissues using an RNA extraction kit (Beyotime, China), and complementary DNA (cDNA) was synthesized using HiScript III RT SuperMix (+gDNA wiper) (Vazyme, China) according to the manufacturer’s instructions. Absolute RT‒qPCR was performed on a 7500 Real-Time PCR System (Applied Biosystems, USA) with ChamQ Universal SYBR qPCR Master Mix (Vazyme, China). The following primers were used: forward primer 5′-AGGAAGTGGAGCAATCAGGAA-3′ and reverse primer 5′-TAACAAGTGGCAGAGCAAAGG-3′.

Western blot analysis

After treatment, the culture supernatants were discarded, and the cells were washed with precooled PBS. Total protein was extracted using RIPA lysis buffer (Solarbio, China) supplemented with a protease phosphatase inhibitor mixture (Beyotime, China). Subsequently, 5× SDS‒PAGE protein loading buffer (Yeasen, China) was added to the protein samples, which were subsequently boiled in a water bath for 10 min. The protein samples were separated by 10% SDS‒PAGE and subsequently transferred to polyvinylidene fluoride membranes (Millipore, USA). The membranes were blocked with 5% skim milk at 37 °C for 2 h and incubated with anti-DTMUV E protein mouse monoclonal antibody (1:1000; our laboratory preparation) or anti-GAPDH mouse monoclonal antibody (1:4000; Proteintech, Cat. No. 60004–1-Ig, China) overnight at 4 °C. The anti-DTMUV E protein monoclonal antibody was generated in our laboratory using recombinant DTMUV E protein domain III as the immunogen. Briefly, mice were immunized with recombinant DTMUV E protein domain III, followed by hybridoma generation, screening, and subcloning of positive hybridoma cells. The selected positive hybridoma clone was expanded to produce the monoclonal antibody, which was subsequently used in this study. After they were washed three times with Tris-buffered saline containing 0.1% Tween 20 (TBST), the membranes were incubated with HRP-conjugated goat anti-mouse IgG (1:4000; Proteintech, Cat. No. SA00001–1, China) at 37 °C for 1 h. After TBST washes, the protein bands were visualized using an ECL Chemiluminescence Kit (Vazyme, China). The band intensities were analysed using ImageJ software.

IFA

At 48 h post-infection, the cells were washed three times with PBS and fixed with cold methanol at 4 °C for 15 min. The cells were then permeabilized with 0.1% Triton X-100 for 15 min and blocked with 1% bovine serum albumin at 37 °C for 1 h. Subsequently, the cells were incubated with anti-DTMUV E protein mouse monoclonal antibody (1:500; our laboratory preparation) at 37 °C for 2 h. After they were washed three times with PBS, the cells were incubated with FITC-conjugated goat anti-mouse IgG (Solarbio, Cat. No. SF131, China) at 37 °C for 1 h in the dark. The nuclei were counterstained with DAPI (Solarbio, China) for 10 min at room temperature. Finally, fluorescence images were captured using a fluorescence microscope (Olympus, Japan).

Direct virucidal assay

To assess the direct inactivation effect of quercetin on DTMUV, the experimental design was established according to previously described procedures (Zhu et al., 2021). In addition to the untreated control group and the virus-infected group, two treatment groups with different intervention strategies were included in this study: (1) Quercetin + virus group: quercetin (40 μM) was mixed with the DTMUV AQ-19 viral suspension and incubated at 37 °C for 1 h. The quercetin-treated viral mixture was subsequently used to infect BHK-21 cells (MOI = 0.1). (2) Quercetin + cell group: BHK-21 cells were pretreated with quercetin (40 μM) at 37 °C for 1 h. Subsequently, the cells were infected with the DTMUV AQ-19 strain at an MOI of 0.1. After infection for 2 h at 37 °C in a humidified 5% CO₂ atmosphere, the inoculum was removed and replaced with DMEM containing 1% FBS, followed by further culture for 48 h.

Adsorption and post-adsorption assay

BHK-21 cells were seeded in 6-well plates and cultured to approximately 80% confluency. In accordance with previously described procedures (Yin et al., 2025), BHK-21 cells were infected with the DTMUV AQ-19 strain (MOI = 0.1) under the following three conditions. For the adsorption assay, BHK-21 cells were infected with DTMUV AQ-19 strain in the presence of quercetin (40 μM) and incubated at 4 °C for 1 h. After incubation, unbound viral particles were removed by washing the cells with cold PBS, followed by the addition of DMEM containing 1% FBS and further incubation at 37 °C for 48 h. For the post-adsorption assay, BHK-21 cells were infected with DTMUV AQ-19 at 4 °C for 1 h. After viral adsorption, the cells were washed with cold PBS, and fresh medium supplemented with 1% FBS and quercetin (40 μM) was added, followed by incubation at 37 °C for 48 h. For the simultaneous treatment, cells were simultaneously infected with DTMUV AQ-19 and treated with quercetin (40 μM) and co-incubated at 37 °C for 48 h.

Molecular docking analysis

The amino acid sequences of DTMUV structural proteins (C, prM, and E) and nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) were retrieved from the NCBI database. Homology modelling was performed using the Swiss-Model online server, and the optimal templates were selected on the basis of sequence identity and global model quality estimation scores to generate three-dimensional protein structures. The resulting models were further optimized using Discovery Studio 2019 by adding hydrogen atoms, repairing missing residues and side chains, and performing energy minimization. The structure of quercetin was obtained from the PubChem database and subjected to energy minimization before it was used as the ligand. Protein and ligand structures were preprocessed and converted into PDBQT files using AutoDock Tools 1.5.6. Molecular docking analysis was subsequently performed using AutoDock Vina 1.2.6, and the conformation with the lowest binding energy was selected as the optimal binding mode.

Animal experiments

Forty healthy 1-day-old goslings were selected from a healthy herd from Anhui Province. All goslings were confirmed to be negative for DTMUV, avian influenza virus, duck reovirus, goose astrovirus and goose parvovirus. Three days later, the goslings were randomly assigned to four groups (n = 10): the control group, DTMUV group, DTMUV + Quercetin (40 mg/kg) group, and DTMUV + Quercetin (80 mg/kg) group. The doses of quercetin (40 and 80 mg/kg) were selected based on previous in vivo studies (Jin et al., 2023; Ma et al., 2015). Two hours before viral challenge, goslings in the DTMUV + Quercetin (40 mg/kg) and DTMUV + Quercetin (80 mg/kg) groups were administered quercetin by oral gavage, whereas goslings in the DTMUV and control groups received an equal volume of sterile PBS containing 0.1% DMSO. Thereafter, treatments were administered once every 24 h. Goslings in the DTMUV group, DTMUV + Quercetin (40 mg/kg) group, and DTMUV + Quercetin (80 mg/kg) group were intramuscularly inoculated with DTMUV at a dose of 10^5.6 TCID₅₀, while goslings in the control group received an equal volume of DMEM. The mortality of each group was monitored and recorded every 24 h for 10 days post-infection, and survival curves were generated on the basis of the recorded data. On day 10 post-infection, all the surviving goslings were euthanized, and liver, spleen, and brain tissues were collected. Viral loads in tissues were determined by RT‒qPCR. Gross pathological changes in each organ were observed and recorded, and tissue samples were subjected to haematoxylin and eosin (H&E) staining.

We confirmed that all the animal experiments were performed in accordance with the Guide for the Care and Use of Laboratory Animals established by Anhui Agricultural University. The protocols were approved by the Animal Care and Use Committee of Anhui Agricultural University.

Statistical analysis

Statistical analysis was performed using GraphPad Prism 10.0 (GraphPad software, USA). The data are presented as the means ± standard deviations (SDs). Comparisons between two groups were analysed using Student’s t-test, while comparisons among multiple groups were performed using one-way analysis of variance (ANOVA). Survival data were analysed using the Log-rank test. A value of p < 0.05 was considered to indicate statistical significance.

Results

Cytotoxic effects of quercetin on BHK-21 cells

A CCK-8 assay was used to detect the cytotoxicity of quercetin on BHK-21 cells. BHK-21 cells were treated with different concentrations of quercetin (0, 5, 10, 20, 40, and 80 μM) for 48 h before the evaluation of cytotoxicity. Compared with the untreated group, BHK-21 cells treated with 5, 10, 20, and 40 μM quercetin did not exhibit obvious cytotoxicity, whereas treatment with 80 μM quercetin inhibited cell proliferation (Fig. 1). Therefore, concentrations of 40 μM quercetin or lower were used in subsequent in vitro cell experiments.

Fig. 1.

Fig. 1

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Quercetin cytotoxic effects on BHK-21 cells. BHK-21 cells were treated with different concentrations of quercetin (0, 5, 10, 20, 40, and 80 μM) for 48 h, and the cytotoxicity of quercetin was measured using a CCK-8 assay. Data are presented as the means ± SDs of three independent experiments. ns, not significant. **** p < 0.0001.

Quercetin inhibits DTMUV replication in BHK-21 cells

To investigate the antiviral effect of quercetin against DTMUV, BHK-21 cells were treated with different concentrations of quercetin (0, 5, 10, 20, and 40 μM) and subsequently infected with DTMUV at an MOI of 0.1. Viral TCID50 in the cell supernatants and viral copy numbers in the cells were determined. The results showed that quercetin reduced the viral titre (Fig. 2A) and viral RNA copy number (Fig. 2B) of DTMUV in a dose-dependent manner. Furthermore, when the concentration of quercetin reached 40 μM, the maximum inhibition rate was approximately 80%, and the half-maximal inhibitory concentration (IC50) was 15.99 μM, with a 95% confidence interval (CI) of 14.79–17.41 μM (Fig. 2C). To further verify the dose-dependent antiviral effect of quercetin against DTMUV, the E protein levels of DTMUV were detected by Western blot analysis and IFA. The results revealed that treatment with quercetin dose-dependently decreased the levels of the DTMUV E protein (Fig. 2D and E).

Fig. 2.

Fig. 2

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Quercetin inhibits DTMUV replication in BHK-21 cells in a dose- and time-dependent manner. BHK-21 cells were pretreated with different concentrations of quercetin (0, 5, 10, 20, and 40 μM) for 2 h before infection with DTMUV (MOI = 0.1) for 48 h. (A) DTMUV viral titers were determined by TCID50 assay. (B) Viral RNA copy numbers were detected by RT‒qPCR. (C) Inhibitory rate of quercetin against DTMUV. Viral inhibition rates were calculated on the basis of the TCID₅₀ results, and the IC₅₀ values were determined by nonlinear regression analysis. (D, E) DTMUV E protein expression was detected by Western blot analysis and IFA. BHK-21 cells were pretreated with quercetin (40 μM) for 2 h before infection with DTMUV (MOI=0.1) for 24, 36, and 48 h. (F) Viral copy numbers were detected by RT‒qPCR. (G) DTMUV E protein expression was detected by Western blotting. Data are presented as the means ± SDs of three independent experiments. ns, not significant. * p < 0.05; *** p < 0.001; **** p < 0.0001.

In addition, BHK-21 cells were treated with 40 μM quercetin followed by DTMUV infection, and viral RNA copy numbers and DTMUV E protein levels were detected at different time points post-infection. The results demonstrated that quercetin significantly inhibited DTMUV replication in BHK-21 cells at 24, 36 and 48 hpi (Fig. 2F and G). These findings indicate that quercetin effectively suppresses DTMUV replication in BHK-21 cells.

Quercetin exhibits direct virucidal activity

To investigate whether quercetin inhibits DTMUV infection in BHK-21 cells by directly targeting viral particles, two different treatment strategies were used. In the Quercetin + virus group, quercetin was incubated with DTMUV at 37 °C for 1 h prior to infection, and the mixture was subsequently used to infect BHK-21 cells for 48 h. In the Quercetin + cell group, BHK-21 cells were pretreated with quercetin at 37 °C for 1 h before DTMUV infection and then incubated for 48 h. Viral titres and replication levels were subsequently determined. As shown in Fig. 3A and B, compared with the untreated DTMUV group, both the Quercetin + virus and Quercetin + cell groups showed significantly reduced viral titres and viral RNA copy numbers. Notably, the inhibitory effect was more pronounced in the Quercetin + virus group than in the Quercetin + cell group.

Fig. 3.

Fig. 3

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Quercetin directly inactivates DTMUV particles. The direct virucidal activity of quercetin against DTMUV was evaluated using two treatment regimens: pre-incubation of quercetin with DTMUV (Quercetin + virus) or pretreatment of cells with quercetin (Quercetin + cell). Cells and culture supernatants were collected at 48 hpi for subsequent analyses. (A) DTMUV viral titres were determined using the TCID₅₀ assay. (B) Viral RNA copy numbers were quantified using RT‒qPCR. (C, D) DTMUV E protein expression was assessed by Western blotting and IFA, respectively. Data are presented as the means ± SDs of three independent experiments. * p < 0.05; ** p < 0.01; **** p < 0.0001.

The expression of the DTMUV E protein was further evaluated by Western blotting and IFA. As shown in Fig. 3C and D, compared with those in the DTMUV group, the DTMUV E protein levels in both quercetin-treated groups markedly decreased, with the inhibitory effect in the Quercetin + virus group being stronger than that in the Quercetin + cell group. Taken together, these results indicate that quercetin exerts a direct virucidal effect on DTMUV particles and can affect the intracellular stages of DTMUV infection.

Quercetin exhibits stronger antiviral activity at the post-adsorption stage of DTMUV infection

To investigate the stage of the DTMUV replication cycle targeted by quercetin, adsorption and post-adsorption assays were performed in BHK-21 cells. As shown in Fig. 4A and B, viral titres and viral RNA copy numbers were significantly lower in the adsorption, post-adsorption, and simultaneous treatment groups than in the untreated control group. Notably, the antiviral effect of quercetin was stronger in the post-adsorption and simultaneous treatment groups than in the adsorption group, with the greatest inhibitory effect observed in the simultaneous treatment group. The expression of the DTMUV E protein was further assessed by Western blotting and IFA. Consistent with the virological results, E protein expression was significantly lower in all quercetin-treated groups than in the DTMUV group, with the most pronounced reduction observed in the simultaneous treatment group (Fig. 4C and D). Collectively, these results indicate that quercetin inhibits DTMUV infection during both the adsorption and post-adsorption stages, with stronger antiviral activity observed during the post-adsorption stage.

Fig. 4.

Fig. 4

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Quercetin has stronger antiviral activity during the post-adsorption stage of DTMUV infection in BHK-21 cells. Three treatment regimens were used to evaluate the antiviral activity of quercetin at different stages of DTMUV infection: (1) Adsorption group: Cells were infected with DTMUV in the presence of quercetin and incubated at 4 °C for 1 h to allow viral adsorption. The medium was then removed and replaced with fresh quercetin-free medium, and the cells were further cultured at 37 °C for 48 h. (2) Post-adsorption group: Cells were infected with DTMUV at 4 °C for 1 h. After viral adsorption, cells were treated with quercetin and cultured at 37 °C for 48 h. (3) Simultaneous treatment group: Cells were infected with DTMUV and treated with quercetin simultaneously at 37 °C for 48 h. (A) DTMUV viral titres were determined using the TCID₅₀ assay. (B) Viral RNA copy numbers were quantified by RT‒qPCR. (C, D) DTMUV E protein expression was analysed by Western blotting and IFA, respectively. The data are presented as the means ± SDs of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Molecular docking predicts quercetin action targets

To predict the binding potential of quercetin to DTMUV proteins, molecular docking analysis was performed using AutoDock Vina. In general, a binding energy lower than −7.0 kcal/mol is considered indicative of good binding affinity between a ligand and its receptor. The docking results revealed that quercetin exhibited the lowest binding energy with the DTMUV non-structural protein NS5, with a binding energy of −8.0 kcal/mol (Fig. 5A), indicating a potential interaction between quercetin and NS5.

Fig. 5.

Fig. 5

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Molecular docking analysis identifies DTMUV NS5 as a potential target of quercetin. Molecular docking analysis was performed using AutoDock Vina to predict the binding affinities of quercetin for DTMUV proteins. (A) The binding energies of the quercetin–protein complexes were predicted using AutoDock Vina 1.2.6. (B) Docking conformations of quercetin with DTMUV structural (C, prM, and E) and nonstructural (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) proteins. Proteins are shown in blue, quercetin is shown in yellow, and hydrogen bonds are shown as pink cartoons.

Further analysis revealed that quercetin formed multiple hydrogen bonds with the NS5 protein. Specifically, the hydroxyl oxygen atom of quercetin formed hydrogen bonds with the backbone amino group of Val545, the side-chain carboxyl group of Glu491, and the side-chain imidazole group of His488, with bond lengths of 2.3 Å, 2.5 Å, and 2.2 Å, respectively (Fig. 5B). These hydrogen bonds were all within favourable interaction distances, with the 2.2 Å hydrogen bond formed with His488 indicating a particularly strong interaction. The formation of multiple hydrogen bonds may contribute to the stability of the quercetin–NS5 complex. Collectively, these findings suggest that NS5 may serve as a potential target through which quercetin exerts its anti-DTMUV activity.

Quercetin alleviates DTMUV-induced infection in goslings

To evaluate the antiviral activity of quercetin against DTMUV in vivo, goslings were treated with quercetin 2 h prior to infection and subsequently challenged with the DTMUV AQ-19 strain. Quercetin was administered daily until day 10 post-infection. The survival time and mortality of goslings in each group were recorded, and the survival curves are shown in Fig. 6A. Compared with those in the DTMUV-infected group, the survival rates of goslings in the DTMUV + Quercetin (80 mg/kg) groups were significantly increased, as determined by the Log-rank test. On day 10 post-infection, five goslings from each group were euthanized for necropsy, and liver, spleen, and brain tissues were collected for further analysis. Gross pathological examination of the liver, spleen, and brain tissues revealed that goslings in the DTMUV group exhibited marked hepatomegaly, a fragile liver texture, yellowish discolouration of the liver surface accompanied by extensive haemorrhagic spots, severe splenomegaly with dark reddish-purple colouration, and aggravated vascular congestion and dilation on the surface of the brain. In contrast, pathological lesions in these tissues were markedly alleviated in the DTMUV + Quercetin (40 mg/kg) and DTMUV + Quercetin (80 mg/kg) groups (Fig. 6B). Viral loads were determined by RT‒qPCR. As shown in Fig. 6C, compared with those in the DTMUV-infected group, viral RNA levels in the tissues of goslings treated with quercetin were significantly lower.

Fig. 6.

Fig. 6

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Quercetin alleviates the severity of DTMUV infection in goslings. Goslings in the quercetin-treated groups were orally administered quercetin 2 h prior to DTMUV infection, followed by administration once every 24 h for 10 consecutive days. Goslings in the control and DTMUV-infected groups received an equal volume of DMSO vehicle. (A) Survival rates of goslings following DTMUV infection (n = 10). At the designated sampling time point, five surviving goslings from each group were randomly selected for subsequent gross pathological examination, viral load determination, and histopathological analysis (n = 5). (B) Representative gross pathological changes in the liver, spleen, and brain. (C) Viral loads in the liver, spleen, and brain were determined by RT-qPCR. Data are presented as the means ± SDs. ns, not significant. * p < 0.05; **** p < 0.0001. (D) Representative H&E-stained liver, spleen, and brain tissue sections were examined under a light microscope (200×). DTMUV infection induced a disorganized hepatocyte arrangement with vascular congestion and inflammatory cell infiltration in the portal area (black arrow), disruption of the splenic architecture with necrotic cells (red arrow), and vascular congestion and dilation (green arrow) accompanied by inflammatory cell infiltration (orange arrow) in the brain.

Furthermore, H&E staining revealed that DTMUV infection induced a disorganized hepatocyte arrangement with vascular congestion and inflammatory cell infiltration in the portal area of the liver. The spleen exhibited disrupted tissue architecture with necrotic cells, while the brain showed marked vascular congestion and dilation accompanied by inflammatory cell infiltration. These pathological changes were significantly alleviated in the DTMUV + Quercetin (40 mg/kg) and DTMUV + Quercetin (80 mg/kg) groups compared with those in the DTMUV group (Fig. 6D). Taken together, these findings demonstrate that quercetin reduces viral burden, attenuates DTMUV-induced tissue damage, and improves the survival of infected goslings, indicating its potent antiviral efficacy in vivo.

Discussion

In the present study, we demonstrated that quercetin exhibits potent antiviral activity against DTMUV both in vitro and in vivo. Quercetin effectively suppressed DTMUV replication in BHK-21 cells by directly inactivating viral particles and disrupting the viral life cycle. Molecular docking analysis suggested that the DTMUV NS5 protein might serve as a potential target of quercetin. Furthermore, in a DTMUV-infected gosling model, quercetin treatment significantly reduced viral loads in multiple tissues, improved survival rates, and mitigated histopathological lesions caused by viral infection. Our findings indicate that quercetin has potential for use as an antiviral agent for the prevention and control of DTMUV infection.

Recent evidence has demonstrated that quercetin possesses significant antiviral properties (Mukherjee and Tripathi, 2025; Yu et al., 2025). However, its antiviral effect against DTMUV remains underexplored. This study revealed that quercetin significantly inhibited DTMUV replication in BHK-21 cells, as evidenced by reduced viral titres, viral RNA levels, and viral E protein expression. Moreover, the antiviral activity of quercetin occurred in a dose- and time-dependent manner, with an IC50 value of 15.99 μM, indicating that quercetin has potent antiviral efficacy against DTMUV in vitro. These findings are consistent with those of previous studies demonstrating the antiviral activity of quercetin against multiple pathogenic viruses (Di Petrillo et al., 2022). For example, quercetin inhibits HSV-1 replication in human corneal epithelial cells (Yu et al., 2025). In dengue virus and zika virus infections, quercetin and its derivatives exhibit significant antiviral activity (Wong et al., 2017; Mukherjee and Tripathi, 2025). In addition, quercetin was shown to inhibit influenza virus replication in Madin-Darby canine kidney cells in a dose-dependent manner (Mehrbod et al., 2020). Our results further support the broad-spectrum antiviral potential of quercetin and indicate that it may serve as an effective antiviral compound against flavivirus infection.

Previous studies have shown that quercetin exerts antiviral effects through multiple mechanisms. One proposed mechanism is the direct targeting of viral surface proteins, thus reducing viral infectivity (Di Petrillo et al., 2022). For example, Lee et al. (2017) reported that quercetin specifically inhibited the expression of HSV-1 glycoprotein D, a critical glycoprotein required for viral entry into host cells, thus impairing viral entry (Lee et al., 2017). Similarly, Wu et al. (2015) demonstrated that quercetin directly interacts with influenza virus particles, particularly the viral haemagglutinin (HA) protein, resulting in the inhibition of viral entry into host cells (Wu et al., 2015). Consistent with these findings, our results from both the direct virucidal assay and the adsorption assay revealed that treatment of DTMUV particles with quercetin significantly reduced viral replication in BHK-21 cells, indicating that quercetin has direct virucidal activity against DTMUV and may exert its antiviral effect by interfering with viral attachment to and entry into cells.

In addition to directly inactivating viral particles, quercetin can exert antiviral effects by targeting post-entry stages of the viral life cycle, including the inhibition of key enzymes involved in viral replication (Nguyen and Bhattacharya, 2022). For example, quercetin suppressed rhinovirus replication in human bronchial epithelial cells by interfering with viral genome transcription (Ganesan et al., 2012). Moreover, quercetin has been reported to suppress hepatitis C virus replication through inhibition of viral NS3 protease activity, highlighting its ability to target the intracellular stages of viral infection (Bachmetov et al., 2012). In the present study, quercetin inhibited DTMUV infection during both the adsorption and post-adsorption stages, with stronger antiviral activity observed during the post-adsorption stage. Given its direct virucidal activity against DTMUV, the antiviral effect detected during the adsorption stage may be partially attributed to direct viral inactivation, whereas the stronger antiviral effect during the post-adsorption stage suggests that quercetin may also interfere with the intracellular events involved in DTMUV replication. Consistent with these observations, molecular docking analysis further suggested that the DTMUV NS5 protein might serve as a potential molecular target of quercetin. NS5 is a key viral protein involved in viral RNA synthesis and RNA capping (Neufeldt et al., 2018). Therefore, the predicted interaction between quercetin and NS5 may provide a potential mechanistic explanation for the inhibitory effect of quercetin during the post-adsorption stage, possibly by interfering with NS5-mediated viral RNA replication and/or capping. However, it should be noted that the molecular docking results only suggest a potential interaction between quercetin and NS5, and further experimental validation is required to confirm whether NS5 is a direct molecular target of quercetin. Moreover, the strongest antiviral activity was observed in the simultaneous treatment group, likely reflecting the combined effects of direct virucidal activity and interference with post-adsorption stages of DTMUV infection. Collectively, these findings suggest that quercetin exerts anti-DTMUV activity through multiple mechanisms, including direct virucidal effects and interference with the intracellular stages of viral infection. However, the precise molecular targets and underlying mechanisms require further investigation.

Although numerous in vitro studies have demonstrated the antiviral activity of quercetin, evidence supporting its antiviral efficacy in vivo is still relatively limited (Di Petrillo et al., 2022). Mukherjee and Tripathi (2025) reported that quercetin significantly reduced dengue virus replication and alleviated vascular leakage and tissue damage in infected mice (Mukherjee and Tripathi, 2025). Similarly, quercetin treatment has been reported to protect mice against pseudorabies virus infection by increasing survival, reducing viral loads in the brain, and alleviating virus-induced histopathological damage (Sun et al., 2021). In this study, quercetin treatment significantly improved survival, reduced viral loads in multiple organs, and alleviated both gross and histopathological lesions, indicating significant anti-DTMUV activity in vivo. The doses of quercetin (40 and 80 mg/kg) used in the present study were determined based on previous studies (Jin et al., 2023; Ma et al., 2015). However, the physiological relevance of these doses and the feasibility of achieving equivalent exposure through dietary supplementation in poultry remain to be determined. In addition, quercetin was administered 2 h before DTMUV challenge in the present study, and thus our animal model primarily evaluated its prophylactic efficacy. Whether quercetin remains effective when administered after DTMUV infection remains unclear. Future studies should therefore investigate post-infection administration to determine its therapeutic efficacy and practical potential for DTMUV control.

In conclusion, this study provides the first systematic evidence that quercetin exerts antiviral activity against DTMUV both in vitro and in vivo. We further demonstrated its antiviral effects at different stages of DTMUV infection, particularly through direct virucidal activity and inhibition of viral replication at the post-adsorption stage. In DTMUV-infected goslings, quercetin suppressed viral replication, reduced viral loads in infected tissues, alleviated histopathological lesions, and increased the survival rate. Furthermore, molecular docking analysis suggested that the DTMUV NS5 may interact with quercetin, providing a potential molecular clue for further investigation of its anti-DTMUV mechanism. Although some of these antiviral properties have been previously reported for quercetin against other viruses, our findings extend its antiviral spectrum to DTMUV both in vitro and in vivo and provide a comprehensive assessment of its inhibitory effects at different stages of DTMUV infection. These findings support further investigation of quercetin as a potential natural antiviral candidate for the prevention and control of DTMUV infection. Future studies are warranted to validate the interaction between quercetin and NS5 and to elucidate the molecular mechanisms underlying its anti-DTMUV activity.

Author Contributions

Jiawen Wang contributed to the study design and core research work, including data acquisition and preliminary data analysis, and drafted the manuscript. Siqi Wang performed the animal experiments, collected data, interpreted the results, and contributed to drafting the manuscript. Kuiru Fang and Yingying Yuan contributed to data analysis, result visualization, and interpretation of the results, and participated in drafting the manuscript. Shinuo Fan made substantial contributions to the study design, experimental methodology, and data analysis. Qing Wang conceived and designed the study, provided overall research supervision, and secured research funding. All authors critically reviewed and revised the manuscript for important intellectual content, approved the exact final version for publication, and agreed to be personally and publicly accountable for all aspects of the work, including ensuring that any questions concerning the accuracy or integrity of the research are appropriately investigated and resolved.

Disclosures

The authors declare that they have no competing interests.

Acknowledgments

This work was supported by the Anhui Provincial Higher Education Scientific Research Projects [Grant No. 2024AH050438], and the Shennong Scholar Project of Anhui Agricultural University [Grant No. rc392101].

Footnotes

Scientific section: Immunology, Health and Disease

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