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. 2025 May 31;104(8):105381. doi: 10.1016/j.psj.2025.105381

Inhibitory effect of curcumin on duck tembusu virus

Dongdong Yin a, Yayun Liu a, Wei Liu a, Guijun Wang b, Lei Yin a, Jieru Wang a, Yin Dai a, Xuehuai Shen a, Ruihong Zhao a, Kai Zhan a, Xiaocheng Pan a,⁎
PMCID: PMC12169727  PMID: 40466261

Abstract

Duck Tembusu virus (DTMUV) is a significant etiological agent responsible for egg production decline in laying ducks and retarded growth in ducklings, contributing to considerable economic losses in the poultry sector. Current research mainly focuses on the development of vaccines for the prevention of DTMUV. However, there is relatively little research on antiviral drugs against this virus. Curcumin has been reported to exert antiviral effects against multiple viruses. However, its efficacy against DTMUV remains unclear. This study aimed to investigate the antiviral activity of curcumin against DTMUV both in vitro and in vivo. Cytotoxicity in BHK-21 cells was assessed utilizing the Cell Counting Kit-8 (CCK-8) assay. The antiviral effects of curcumin were evaluated using viral titration, qRT-PCR, Western blotting, and indirect immunofluorescence. In addition, a DTMUV-infected duck model was used to assess the therapeutic potential of curcumin in vivo. The experimental results indicated that curcumin was non-toxic to BHK-21 cells at concentrations up to 30 μM. In vitro, curcumin significantly reduced DTMUV replication in a dose-dependent manner, as confirmed by decreased viral titers, RNA copy numbers, and E protein expression. Further analysis revealed that curcumin exerted its antiviral effect primarily at the post-adsorption stage of the viral life cycle. In vivo, curcumin treatment improved the survival rate of DTMUV-infected ducklings and alleviated virus-associated pathology. These findings demonstrate that curcumin effectively inhibits DTMUV infection and highlight its potential as a viable candidate for the prevention and treatment of DTMUV-related diseases.

Keywords: Duck tembusu virus, Curcumin, Antiviral activity, Virus replication

Introduction

Duck Tembusu virus (DTMUV), a single-stranded positive-sense RNA virus belonging to the Flavivirus genus within the Flaviviridae family, has posed a serious threat to China's waterfowl industry since its emergence in 2010(Cao, et al., 2011; Tang, et al., 2012). Infection in breeders and laying ducks results in fever, paralysis, neurological symptoms, and a sharp decline in egg production, significantly impairing reproductive performance (Li, et al., 2012; Liu, et al., 2013; Yan, et al., 2011). As a Flavivirus member, DTMUV has a broad host range, including mosquitoes, wild birds, and humans, thereby presenting considerable public health risks (Pulmanausahakul, et al., 2022; Sanisuriwong, et al., 2020; Tang, et al., 2013). In China, prevention relies on vaccination, supported by biosecurity measures, to control viral spread and mitigate economic losses. Although commercial vaccines provide partial protection, the extensive genetic diversity among circulating DTMUV strains limits their effectiveness in preventing outbreaks. Continued research is required to develop safe, stable, and effective vaccines or antiviral agents with low toxicity.

Curcumin, a bioactive compound derived from the rhizome of Curcuma longa, is widely utilized as a food colorant and flavoring agent (Kotha and Luthria, 2019). Extensive research has demonstrated its broad biological activities, including antioxidant, antiviral, and antitumor properties (Butnariu, et al., 2022; Lao, et al., 2006; Mirzaei, et al., 2017). Its antiviral efficacy has been validated against several Flavivirus members, such as, Japanese encephalitis virus (JEV), and dengue virus (DENV) (Dutta, et al., 2009; Mounce, et al., 2017; Nabila, et al., 2020; Obłoza, et al., 2024). However, its effect on the Duck Tembusu virus (DTMUV) remains unexplored. This study explores the inhibitory effects of curcumin on DTMUV replication, offering foundational evidence for the design of new antiviral strategies against this virus.

Materials and Methods

Virus, cells, and antibodies

The DTMUV AQ-19 strain (GenBank accession no. MT708901) (Zhu, et al., 2022) was provided by Professor Guijun Wang from Anhui Agricultural University. BHK-21 cells were maintained in Dulbecco’s Modified Eagle Medium (DMEM; Gibco, USA) enriched with 10% FBS (Gibco, USA) and incubated at 37 °C in a humidified atmosphere containing 5% CO₂. Curcumin was purchased from MedChemExpress (MCE, China), dissolved in DMSO (Solarbio, China), and stored at 4 °C.

Cytotoxicity assay of curcumin

To determine the cytotoxicity of curcumin, a Cell Counting Kit-8 (CCK-8) assay (Beyotime, China) was performed. BHK-21 cells were seeded into 96-well plates and cultured until confluency. Various concentrations of curcumin (0, 10, 20, 30, 40, and 50 μM) were added in sextuplicate. After a 48-hour incubation, 10 μL of CCK-8 reagent was introduced to each well, followed by a 2-hour reaction period. Cell viability was then determined by measuring absorbance at 450 nm using a microplate reader.

In vitro antiviral activity of curcumin against DTMUV

BHK-21 cells were seeded into 12-well plates and cultured until reaching approximately 90% confluency. Cells were then infected with the DTMUV AQ-19 strain at a multiplicity of infection (MOI) of 0.1, followed by treatment with various concentrations of curcumin (0 μM, 7.5 μM, 15 μM, 22.5 μM, 30 μM). Supernatants were collected to determine viral titers, and cells were harvested for quantification of viral RNA copies using RT-qPCR. In addition, expression of the DTMUV envelope (E) protein was assessed through Western blotting and indirect immunofluorescence assay (IFA).

Adsorption and postadsorption assays

BHK-21 cells were plated in 12-well culture plates and grown to approximately 90% confluency. For the adsorption assay, DTMUV AQ-19 (MOI = 0.1) was mixed with curcumin and co-incubated with the cells at 4 °C for 1 hour to allow viral binding. After incubation, the supernatant was removed by washing with PBS, and fresh 1% DMEM was added. The cells were then incubated at 37 °C in 5% CO₂ for 48 hours. In the post-adsorption group, cells were first exposed to DTMUV AQ-19 at 4 °C for 1 hour. After viral adsorption, cells were washed with PBS and treated with curcumin-containing DMEM, followed by incubation at 37 °C for 48 hours. For the simultaneous treatment group, cells were exposed to DTMUV AQ-19 with curcumin at 37 °C and incubated for 48 hours.

In vivo antiviral activity of curcumin against DTMUV

Forty 7-day-old ducklings confirmed to be seronegative for DTMUV antibodies were randomly assigned into four groups (n = 10). In the DTMUV group, each duck received an intramuscular injection of DTMUV AQ-19 at a dose of 105.0 TCID₅₀. Ducks in the control group were intramuscularly injected with the same volume of PBS containing 0.1% DMSO, serving as negative controls. Ducks in the DTMUV + curcumin (200 mg/kg) and DTMUV + curcumin (400 mg/kg) groups were orally administered curcumin at the indicated doses. Treatment began 4 hours after the viral challenge. Upon death, liver, spleen, and brain tissues were collected for histopathological examination and RT-qPCR analysis of viral RNA levels. Surviving ducks were euthanized two weeks after infection, and tissue samples were harvested for further evaluation. Histopathological damage score (proportion of damaged tissue in the field of view): 0 points indicates no damage; 1 point indicates the damage proportion is <25%; 2 points indicates the damage proportion is 25% - 50%; 3 points indicates the damage proportion is 51% - 75%; 4 points indicates the damage proportion is >76%. All procedures were conducted with approval from the Animal Ethics Committee of the Anhui Academy of Agricultural Sciences.

Quantitative Real-Time PCR for DTMUV Detection

Quantification of DTMUV RNA copies was performed by qRT-PCR following the protocol described by Zhu (Zhu, et al., 2021). Total RNA was isolated from BHK-21 cells utilizing an RNA extraction kit (Beyotime, China), and reverse transcription was carried out with a cDNA synthesis kit from the same manufacturer. Absolute quantification of viral RNA (vRNA) load was performed utilizing SYBR Green-based qPCR master mix (Mei5 Biotechnology, China).

Western Blot

Western blotting was performed to evaluate the expression of the DTMUV envelope (E) protein in BHK-21 cells. At 48 hours post-infection, cells were lysed using RIPA buffer (Beyotime, China) to extract total proteins, which were then resolved by SDS-PAGE and transferred onto PVDF membranes. The membranes were incubated overnight at 4 °C with monoclonal antibodies targeting DTMUV E protein (Lv, et al., 2021) and β-actin. Following washing, HRP-labeled goat anti-mouse IgG (Beyotime, China) was applied at 37 °C for 1 hour. Protein signals were detected using enhanced chemiluminescence (ECL) reagents (Beyotime, China), and band intensities were quantified using ImageJ software (NIH, USA).

Indirect immunofluorescence assay

Indirect IFA was used to evaluate DTMUV E protein expression in BHK-21 cells. Cells were fixed with paraformaldehyde and rinsed with PBS before incubation with anti-DTMUV E protein monoclonal antibodies at 37 °C for 1 hour. After additional PBS washes, Alexa Fluor 488-labeled goat anti-mouse IgG was applied under the same conditions. Nuclei were counterstained with DAPI (Antgene, China), and fluorescence was observed utilizing an Olympus fluorescence microscope (Olympus Inc, Japan).

Statistical analysis

Data were analyzed utilizing GraphPad Prism 9.0 (GraphPad Software, USA). Comparisons between groups were performed utilizing one-way ANOVA, Student’s t-test, or Log-rank test, depending on the context. Differences with p-values below 0.05 were considered statistically significant.

Results

Cytotoxicity of curcumin on BHK-21 cells

The cytotoxic effects of curcumin on BHK-21 cells at different concentrations are shown in Fig. 1. When the concentration of curcumin was below 30 μM, cell viability remained above 80%, indicating no significant cytotoxicity. However, higher concentrations (40–50 μM) caused a marked reduction in cell viability compared with lower doses. Based on these results, 30 μM was selected as the maximum concentration for subsequent experiments.

Fig. 1.

Fig 1

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Cytotoxic effect of curcumin on BHK-21 cells. BHK-21 cells were treated with curcumin at concentrations ranging from 0 to 50 μM for 48 h, and cell viability was assessed using the CCK-8 assay. Data are presented as mean ± SD from three independent experiments. *P < 0.05, **P < 0.01.

Dose-dependent inhibitory effect of curcumin on DTMUV

To assess the inhibitory effect of curcumin on DTMUV replication, BHK-21 cells were exposed to different concentrations of curcumin (0, 7.5, 15, 22.5, and 30 μM) before infection with DTMUV at an MOI of 0.1. Viral titers in culture supernatants and intracellular viral RNA levels were subsequently measured. As illustrated in Fig. 2A and 2B, both viral titers and RNA levels reduced dose-dependent with increasing concentrations of curcumin. The maximum inhibition rate at 30 μM reached approximately 80%, and the half-maximal inhibitory concentration (IC₅₀) was calculated to be 21.99 μM (Fig. 2C). In addition, to further confirm the antiviral effect of curcumin, the DTMUV E protein in BHK-21 cells was evaluated by Western blot and indirect IFA. As shown in Fig. 2D and 2E, E protein levels reduced dose-dependently following curcumin treatment. These findings indicate that curcumin effectively inhibits DTMUV replication in BHK-21 cells.

Fig. 2.

Fig 2

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Dose-dependent inhibitory effect of curcumin on DTMUV infection in BHK-21 cells. Cells were pretreated with curcumin at concentrations (0, 7.5, 15, 22.5, and 30 μM) and infected with DTMUV (MOI = 0.1) for 48 h. (A) Viral titers were determined by TCID₅₀ assay. (B) Viral RNA copy numbers were quantified by qRT-PCR. (C) The inhibition rate was calculated based on progeny virus titers. (D, E) Expression of the DTMUV E protein was detected by Western blot and indirect immunofluorescence assay (IFA), respectively. Data are shown as mean ± SD from three independent experiments.

Curcumin inhibits DTMUV infection at the post-adsorption stage in BHK-21 cells

To identify the stage of the DTMUV replication cycle targeted by curcumin, adsorption and post-adsorption assays were conducted in BHK-21 cells. Compared with the DTMUV-infected group, viral titers and RNA copy numbers were reduced to varying degrees in the Simultaneous, Adsorption, and Post-adsorption groups. Notably, the Simultaneous and Post-adsorption groups exhibited significant antiviral effects relative to the DTMUV group (Fig. 3A and 3B). Western blotting and immunofluorescence analysis further confirmed that DTMUV E protein expression was markedly decreased in both the Simultaneous and Post-adsorption groups compared with the untreated infection group (Fig. 3C and 3D). These results suggest that curcumin predominantly inhibits DTMUV infection by interfering with the post-adsorption stage of the viral life cycle.

Fig. 3.

Fig 3

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Curcumin inhibits DTMUV infection by blocking the post-adsorption stage in BHK-21 cells. Cells were subjected to three treatment conditions: (1) Simultaneous treatment group: cells were co-treated with 30 μM curcumin and DTMUV (MOI = 0.1) at 37 °C; (2) Adsorption group: cells were incubated with DTMUV and 30 μM curcumin at 4 °C for 1 h, followed by replacement with curcumin-free DMEM and incubation for 48 h; (3) Post-adsorption group: cells were first adsorbed with DTMUV at 4 °C for 1 h, then treated with 30 μM curcumin at 37 °C for 48 h. (A) Viral titers were assessed by TCID₅₀ assay. (B) Viral RNA levels were measured by qRT-PCR. (C, D) DTMUV E protein expression was evaluated by Western blot and IFA, respectively. Data are presented as mean ± SD from three independent experiments.

Curcumin inhibits DTMUV infection in vivo

To evaluate the in vivo antiviral efficacy of curcumin, treatment was initiated 4 h after DTMUV infection in ducklings. As shown in Fig. 4A, both 200 mg/kg and 400 mg/kg curcumin treatments significantly improved survival rates compared with the DTMUV group (Log-rank test, P < 0.05 and P < 0.01, respectively). At 14 days post-infection, a necropsy was performed to assess pathological changes. Ducklings in the DTMUV-infected group exhibited yellowish livers, splenomegaly, and severe meningeal congestion and hemorrhage. In contrast, these pathological features were absent in the curcumin-treated and control groups, with the liver, spleen, and brain appearing grossly normal (Fig. 4B). Viral RNA levels in the liver, spleen, and brain were significantly elevated in DTMUV-infected ducklings compared with the control group. Notably, curcumin-treated groups showed markedly reduced viral copy numbers in these tissues relative to the DTMUV group (Fig. 4C).

Fig. 4.

Fig 4

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In vivo antiviral effect of curcumin against DTMUV infection. Ducklings were infected with DTMUV 4 h before curcumin administration. (A) Survival rates were monitored for 14 days. The survival curves were compared using the Log-rank test. ∗∗P < 0.001; ∗P < 0.05. (B) Gross pathological changes in each group were recorded during necropsy. (C) Viral RNA copy numbers in the liver, spleen, and brain were measured by qRT-PCR. Tissues were collected at 14 dpi for surviving ducklings. Data represent mean ± SD from three independent experiments.

The histopathological analysis further revealed that DTMUV infection induced vacuolar degeneration in hepatocytes. In contrast, curcumin-treated ducklings exhibited only mild histopathological changes in the liver, suggesting a protective effect against DTMUV-induced hepatic injury. In the spleen, hematoxylin-eosin (H&E) staining showed prominent cellular necrosis following DTMUV infection, whereas tissue damage was significantly alleviated in both low- and high-dose curcumin-treated groups. The histopathological score statistics of the liver, brain and spleen showed that the scores in the DTMUV group were significantly higher than those in the control group, while the scores in the 200 mg/kg and 400 mg/kg curcumin treatment groups were significantly lower than those in the DTMUV group (Fig. 5). These findings indicate that curcumin confers protective effects against DTMUV infection in vivo.

Fig. 5.

Fig 5

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Histopathological examination of liver, spleen, and brain tissues from DTMUV-infected ducklings treated with curcumin. Tissues were stained with hematoxylin and eosin (H&E) and observed under light microscopy at 200 × magnification. DTMUV infection induced vacuolar degeneration in hepatocytes (black arrow), cerebral vascular dilation (green arrow), and prominent cellular necrosis in the spleen (red arrow). ∗∗P < 0.001.

Discussion

This study demonstrated that curcumin effectively suppressed DTMUV replication in BHK-21 cells. These effects were mainly attributed to its virucidal properties and its ability to prevent viral entry and internalization into host cells. These results suggest that curcumin holds therapeutic potential for the treatment of DTMUV infection.

Current research has demonstrated that curcumin possesses notable antiviral activity against various viruses. Marín-Palma reported that curcumin exhibited significant in vitro antiviral effects against SARS-CoV-2, with efficacy maintained across various strains and variants (Marín-Palma, et al., 2021). Maurya further showed that curcumin forms hydrogen bonds with key residues of the SARS-CoV-2 spike protein (e.g., Lys304, Arg765) and its receptor ACE2 (e.g., His378, Asn394), thereby disrupting virus-host cell interactions and inhibiting viral replication (Maurya, et al., 2020). In addition, Li demonstrated that curcumin exerts direct virucidal effects against transmissible gastroenteritis virus (TGEV), primarily by interfering with the viral adsorption stage (Li, et al., 2020). No previous research has addressed the antiviral effect of curcumin against DTMUV. The present study confirmed that curcumin effectively suppresses DTMUV replication, as indicated by reductions in viral titers, RNA copy numbers, and DTMUV E protein expression levels. Both in vitro and in vivo experiments demonstrated that curcumin treatment significantly prevents DTMUV infection.

Previous studies have reported that curcumin inhibits viral infections through multiple mechanisms. For example, curcumin interferes with the early stages of the replication cycle of Japanese encephalitis and vesicular stomatitis virus. Another study demonstrated that curcumin disrupts the conformation of the DENV NS2B-NS3 protease, thereby inhibiting its enzymatic activity and blocking DENV infection (Gangopadhyay and Saha, 2023). Wei found that curcumin suppresses hepatitis B virus infection by downregulating histone acetylation associated with cccDNA binding (Wei, et al., 2017). Prasad confirmed that curcumin inhibits both the protease and integrase of human immunodeficiency virus (HIV), suppresses transactivation of the HIV receptor genome, and reduces viral production in infected cells (Prasad and Tyagi, 2015). The findings of the present study indicate that the antiviral activity of curcumin against DTMUV may be mediated by interference with viral internalization and entry.

In conclusion, curcumin demonstrates notable antiviral activity against DTMUV by markedly inhibiting viral replication. These results strongly support curcumin as a potential therapeutic candidate for treating and controlling DTMUV infection, highlighting the need for further exploration of its clinical applicability. Moreover, the present study demonstrates that curcumin is effective at multiple doses in ducks. Nevertheless, comprehensive studies on the safety and pharmacokinetics of curcumin in ducks are required to facilitate its future application in veterinary settings.

Declaration of competing interest

The authors declare no competing interests.

Acknowledgments

This study was supported financially by the China Agriculture Research System of MOF and MARA (grant number: CARS-40), the Achievement Transformation Project of Anhui Academy of Agricultural Sciences (grant number: 2025ZH025).

References

  1. Butnariu M., Quispe C., Koirala N., Khadka S., Salgado-Castillo C.M., Akram M., Anum R., Yeskaliyeva B., Cruz-Martins N., Martorell M., Kumar M., Vasile Bagiu R., Abdull Razis A.F., Sunusi U., Muhammad Kamal R., Sharifi-Rad J. Bioactive effects of curcumin in Human immunodeficiency virus infection along with the most effective isolation techniques and type of nanoformulations. Int. J. Nanomed. 2022;17:3619–3632. doi: 10.2147/ijn.S364501. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Cao Z., Zhang C., Liu Y., Liu Y., Ye W., Han J., Ma G., Zhang D., Xu F., Gao X., Tang Y., Shi S., Wan C., Zhang C., He B., Yang M., Lu X., Huang Y., Diao Y., Ma X., Zhang D. Tembusu virus in ducks, china. Emerg. Infect. Dis. 2011;17:1873–1875. doi: 10.3201/eid1710.101890. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Dutta K., Ghosh D., Basu A. Curcumin protects neuronal cells from Japanese encephalitis virus-mediated cell death and also inhibits infective viral particle formation by dysregulation of ubiquitin-proteasome system. J. Neuroimmune Pharmacol. 2009;4:328–337. doi: 10.1007/s11481-009-9158-2. [DOI] [PubMed] [Google Scholar]
  4. Gangopadhyay A., Saha A. Exploring allosteric hits of the NS2B-NS3 protease of DENV2 by structure-guided screening. Comput. Biol. Chem. 2023;104 doi: 10.1016/j.compbiolchem.2023.107876. [DOI] [PubMed] [Google Scholar]
  5. Kotha R.R., Luthria D.L. Curcumin: biological, pharmaceutical, nutraceutical, and analytical aspects. Molecules. 2019;24 doi: 10.3390/molecules24162930. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Lao C.D., Ruffin M.T.T., Normolle D., Heath D.D., Murray S.I., Bailey J.M., Boggs M.E., Crowell J., Rock C.L., Brenner D.E. Dose escalation of a curcuminoid formulation. BMC Complement. Altern. Med. 2006;6:10. doi: 10.1186/1472-6882-6-10. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Li L., An H., Sun M., Dong J., Yuan J., Hu Q. Identification and genomic analysis of two duck-origin Tembusu virus strains in southern China. Virus Genes. 2012;45:105–112. doi: 10.1007/s11262-012-0753-6. [DOI] [PubMed] [Google Scholar]
  8. Li Y., Wang J., Liu Y., Luo X., Lei W., Xie L. Antiviral and virucidal effects of curcumin on transmissible gastroenteritis virus in vitro. J. Gen. Virol. 2020;101:1079–1084. doi: 10.1099/jgv.0.001466. [DOI] [PubMed] [Google Scholar]
  9. Liu P., Lu H., Li S., Wu Y., Gao G.F., Su J. Duck egg drop syndrome virus: an emerging Tembusu-related flavivirus in China. Sci. China Life Sci. 2013;56:701–710. doi: 10.1007/s11427-013-4515-z. [DOI] [PubMed] [Google Scholar]
  10. Lv X., Zhang M., Yu S., Zhang C., Fang T., Liu D., Jia B., Zhu M., Wang B., Wang Q., Zhu Y., Wang G. Antiviral and virucidal activities of lycorine on duck tembusu virus in vitro by blocking viral internalization and entry. Poult. Sci. 2021;100 doi: 10.1016/j.psj.2021.101404. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Marín-Palma D., Tabares-Guevara J.H., Zapata-Cardona M.I., Flórez-Álvarez L., Yepes L.M., Rugeles M.T., Zapata-Builes W., Hernandez J.C., Taborda N.A. Curcumin inhibits In Vitro SARS-CoV-2 infection In Vero E6 cells through multiple antiviral mechanisms. Molecules. 2021;26 doi: 10.3390/molecules26226900. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Maurya V.K., Kumar S., Prasad A.K., Bhatt M.L.B., Saxena S.K. Structure-based drug designing for potential antiviral activity of selected natural products from Ayurveda against SARS-CoV-2 spike glycoprotein and its cellular receptor. Virusdisease. 2020;31:179–193. doi: 10.1007/s13337-020-00598-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Mirzaei H., Shakeri A., Rashidi B., Jalili A., Banikazemi Z., Sahebkar A. Phytosomal curcumin: a review of pharmacokinetic, experimental and clinical studies. Biomed. Pharmacother. 2017;85:102–112. doi: 10.1016/j.biopha.2016.11.098. [DOI] [PubMed] [Google Scholar]
  14. Mounce B.C., Cesaro T., Carrau L., Vallet T., Vignuzzi M. Curcumin inhibits Zika and chikungunya virus infection by inhibiting cell binding. Antiviral Res. 2017;142:148–157. doi: 10.1016/j.antiviral.2017.03.014. [DOI] [PubMed] [Google Scholar]
  15. Nabila N., Suada N.K., Denis D., Yohan B., Adi A.C., Veterini A.S., Anindya A.L., Sasmono R.T., Rachmawati H. Antiviral Action of Curcumin Encapsulated in Nanoemulsion against Four Serotypes of Dengue Virus. Pharm. Nanotechnol. 2020;8:54–62. doi: 10.2174/2211738507666191210163408. [DOI] [PubMed] [Google Scholar]
  16. Obłoza M., Milewska A., Botwina P., Szczepański A., Medaj A., Bonarek P., Szczubiałka K., Pyrć K., Nowakowska M. Curcumin-poly(sodium 4-styrenesulfonate) conjugates as potent Zika virus entry inhibitors. ACS Appl. Mater. Interfac. 2024;16:5426–5437. doi: 10.1021/acsami.3c13893. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Prasad S., Tyagi A.K. Curcumin and its analogues: a potential natural compound against HIV infection and AIDS. Food Funct. 2015;6:3412–3419. doi: 10.1039/c5fo00485c. [DOI] [PubMed] [Google Scholar]
  18. Pulmanausahakul R., Ketsuwan K., Jaimipuk T., Smith D.R., Auewarakul P., Songserm T. Detection of antibodies to duck tembusu virus in human population with or without the history of contact with ducks. Transbound. Emerg. Dis. 2022;69:870–873. doi: 10.1111/tbed.13998. [DOI] [PubMed] [Google Scholar]
  19. Sanisuriwong J., Yurayart N., Thontiravong A., Tiawsirisup S. Duck Tembusu virus detection and characterization from mosquitoes in duck farms. Thailand. Transbound. Emerg. Dis. 2020;67:1082–1088. doi: 10.1111/tbed.13474. [DOI] [PubMed] [Google Scholar]
  20. Tang Y., Diao Y., Gao X., Yu C., Chen L., Zhang D. Analysis of the complete genome of Tembusu virus, a flavivirus isolated from ducks in China. Transbound. Emerg. Dis. 2012;59:336–343. doi: 10.1111/j.1865-1682.2011.01275.x. [DOI] [PubMed] [Google Scholar]
  21. Tang Y., Diao Y., Yu C., Gao X., Ju X., Xue C., Liu X., Ge P., Qu J., Zhang D. Characterization of a Tembusu virus isolated from naturally infected house sparrows (Passer domesticus) in Northern China. Transbound. Emerg. Dis. 2013;60:152–158. doi: 10.1111/j.1865-1682.2012.01328.x. [DOI] [PubMed] [Google Scholar]
  22. Wei Z.Q., Zhang Y.H., Ke C.Z., Chen H.X., Ren P., He Y.L., Hu P., Ma D.Q., Luo J., Meng Z.J. Curcumin inhibits hepatitis B virus infection by down-regulating cccDNA-bound histone acetylation. World J. Gastroenterol. 2017;23:6252–6260. doi: 10.3748/wjg.v23.i34.6252. [DOI] [PMC free article] [PubMed] [Google Scholar]
  23. Yan P., Zhao Y., Zhang X., Xu D., Dai X., Teng Q., Yan L., Zhou J., Ji X., Zhang S., Liu G., Zhou Y., Kawaoka Y., Tong G., Li Z. An infectious disease of ducks caused by a newly emerged Tembusu virus strain in mainland China. Virology. 2011;417:1–8. doi: 10.1016/j.virol.2011.06.003. [DOI] [PubMed] [Google Scholar]
  24. Zhu Y., Gu X., Zhang M., Lv X., Zhang C., Li J., Hu Z., Wu Q., Zhang R., Wei J., Huang R., Wang B., Wang Q., Wang G. Epigallocatechin-3-gallate exhibits antiviral effects against the duck Tembusu virus via blocking virus entry and upregulating type I interferons. Poult. Sci. 2021;100 doi: 10.1016/j.psj.2021.01.012. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Zhu Y., Hu Z., Lv X., Huang R., Gu X., Zhang C., Zhang M., Wei J., Wu Q., Li J., Zhang R., Cao S., Yin D., Wang B., Liu G., Wang G. A novel Tembusu virus isolated from goslings in China form a new subgenotype 2.1.1. Transbound. Emerg. Dis. 2022;69:1782–1793. doi: 10.1111/tbed.14155. [DOI] [PubMed] [Google Scholar]

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