BMC Veterinary Research
·
2024
·Vol. 20
·期 1
·1-11
·
IF 2.3
Yang Yuxin,Hu XianWang,Wang Shuangshuang,Tian Yongxiang,Yang Keli,Li Chang,Wu Qiong,Liu Wei,Gao Ting,Yuan Fangyan,Guo Rui,Liu Zewen,Yang Yuying,Zhou Danna
Background Japanese encephalitis virus (JEV) is a mosquito-borne zoonotic pathogen that causes encephalitis in humans and reproductive failure in pigs. The transmission of JEV between humans and animals poses a significant public health threat and results in substantial economic losses. Excessive inflammation in the central nervous system of JEV-infected patients is a major cause of mortality and disability. Rosmarinic acid (RA), a polyhydroxyphenolic compound isolated from medicinal herbs, has been preliminarily shown to possess anti-inflammatory properties and significantly inhibit JEV-induced neuroinflammation in mice. Results This study investigated the antiviral capacity and potential mechanisms of RA in JEV-infected cells. The results demonstrated that RA could inhibit JEV replication in vitro. Furthermore, the expression levels of inflammatory cytokines (including IL-6, IL-1β, CCL-2, and TNF-α), membrane receptors (including RIG-I, TLR3, TLR4, TLR7, and TLR8), NF-κB complex and p62/SQSTM1 were assessed using qPCR, ELISA, and Western blot, respectively. The findings indicated that RA significantly suppressed the expression of IL-6, IL-1α, TNF-α, and CCL-2 in JEV-infected BV-2 cells in a dose-dependent manner. Additionally, RA treatment downregulated the expression levels of RIG-I and p62, while p62 silencing inhibited the upregulation of inflammatory cytokines in JEV-infected BV-2 cells. Conclusion Our present study highlights the important role of RA-mediated reduction of RIG-I and p62 in microglia, conferring resistance to Japanese encephalitis virus-induced inflammation.
研究领域:
病毒学
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免疫学
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药理学
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DOI
PubMed
高影响因子
NEW JOURNAL OF CHEMISTRY
·
2018
·Vol. 42
·期 5
·3503-3508
·
IF 3.201
Wenbao Feng,Caishuang Liang,Hang Gong,Changqun Cai
This study demonstrated fluorescent detection of Japanese encephalitis virus (JEV) by surface molecularly imprinted technique. After dansyl chloride (DNS-Cl) was immobilized on silica microspheres (SiMP) with JEV as the template, (3-aminopropyl)triethoxysilane (APTES) as the monomer and tetraethyl orthosilicate (TEOS) as the cross-linker was mixed with SiMP, and the polymerization was performed in mild condition. After polymerization, templates were removed to obtain JEV-imprinted polymers (JEV-MIPs). The obtained JEV-MIPs can selectively recognize JEV in the presence of Hepatitis A virus (HAV), Simian virus 40 (SV40) and Rabies virus (RV), and also sensitively detect JEV with a picomolar detection limit.
研究领域:
病毒学
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生物医学工程
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分析化学
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产品关联
DOI
高影响因子
TALANTA
·
2016
·
IF 4.035
Caishuang Liang,Huan Wang,Kui He,Chunyan Chen,Xiaoming Chen,Hang Gong,Changqun Cai
Major stumbling blocks in the recognition and detection of virus are the unstable biological recognition element or the complex detection means. Here a fluorescent sensor based on virus-molecular imprinted polymers (virus-MIPs) was designed for specific recognition and highly sensitive detection of Japanese encephalitis virus (JEV). The virus-MIPs were anchored on the surface of silica microspheres modified by fluorescent dye , pyrene-1-carboxaldehyde (PC). The fluorescence intensity of PC can be enhanced by the principle of fluorescence resonance energy transfer (FRET), where virus acted as energy donor and PC acted as energy acceptor. The enhanced fluorescence intensity was proportional to the concentration of virus in the range of 24–960 pM, with a limit of detection (LOD, 3σ) of 9.6 pM, and the relative standard deviation was 1.99%. In additional, the specificity study confirmed the resultant MIPs has high-selectivity for JEV. This sensor would become a new key for the detection of virus because of its high sensitive, simple operation, high stability and low cost.
研究领域:
生物化学
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分析化学
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病毒学
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产品关联
DOI
PubMed
高影响因子
VIROLOGY
·
2023
·
IF 3.7
Xiaoyan Zheng,Ran Wang,Chenghong Yin
Dengue virus (DENV), Japanese encephalitis virus (JEV) and Zika virus (ZIKV) are the three most important flaviviruses, which can cause health problems worldwide. All these flaviviruses can cause liver damage, however, the mechanism of liver injury is still unclear. Metabolomics can give insight into the full complexity of a disease. In our study, we used an LC-MS method to analysis the metabolites in liver samples of the three flaviviruses-infected mice and the non-infected mice. Compared with the control mice, the liver of the DENV-infected, JEV-infected, and ZIKV-infected mice had 32, 34, and 55 differential metabolites. We also found that there were obvious differences in some metabolic pathways among the four groups. Metabonomic analysis of liver is very important for understanding the pathogenesis of flaviviruses.
研究领域:
病毒学
·
医学
·
代谢组学
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DOI
PubMed
高影响因子
VETERINARY MICROBIOLOGY
·
2024
·
IF 2.4
Le-le Liu,You-qin Yin,Kai-xiong Ma,Jin-chao Xing,Xing-xing Ren,Jin-yu Huang,Ming Liao,Wen-bao Qi,Li-hong Huang
Japanese encephalitis virus (JEV) is a pathogen with a substantial impact on both livestock and human health. However, the critical host factors in the virus life cycle remain poorly understood. Using a library comprising 123411 small guide RNAs (sgRNAs) targeting 19050 human genes, we conducted a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-based screen to identify essential genes for JEV replication. By employing knockout or knockdown techniques on genes, we identified eleven human genes crucial for JEV replication, such as prolactin releasing hormone receptor (PRLHR), activating signal cointegrator 1 complex subunit 3 (ASCC3), acyl-CoA synthetase long chain family member 3 (ACSL3), and others. Notably, we found that PRLHR knockdown blocked the autophagic flux, thereby inhibiting JEV infection. Taken together, these findings provide effective data for studying important host factors of JEV replication and scientific data for selecting antiviral drug targets.
研究领域:
病毒学
·
分子生物学
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基因组学
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产品关联
DOI
PubMed
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
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2016
·
IF 4.758
Kui He,Chunyan Chen,Caishuang Liang,Chan Liu,Bin Yang,Xiaoming Chen,Changqun Cai
A novel virus-recognition fluorescent sensor based on virus-imprinted polymers (VIP) for highly selective and highly sensitive detection of Japanese encephalitis virus (JEV) was presented. The virus-imprinted method went beyond simple shape imprinting through surface imprinting with magnetic silicon microspheres acting as carrier materials and tetraethyl orthosilicate (TEOS) functioning as building blocks. The resulting VIP film could selectively capture target JEV via recognition cavities, and a high imprinting factor of 2.98 was achieved. Furthermore, fast magnetic separation and highly sensitive fluorescent detection in water were offered for JEV, showing a good linearity within 2.5–45 nM ( R 2 = 0.9948). Finally, the specificity study confirmed that the virus-imprinted magnetic silicon microspheres demonstrated excellent selectivity for JEV in several different types of virus.
研究领域:
生物传感器技术
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病毒学
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产品关联
DOI
高影响因子
JOURNAL OF CONTROLLED RELEASE
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2020
·
IF 7.727
Yanchao Liu,Yi Han,Ting Fang,Si-Min Chen,Xinyu Hu,Lijun Song,Hui Shen,Haiqing Dong,Yuan-Ying Jiang,Zui Zou,Yongyong Li,Mao-Mao An
As the gold standard treatment for invasive fungal infection , amphotericin B (AmB) is limited by its severe nephrotoxicity . It has been shown that AmB complex with albumin in vivo forms a sub-10 nm nanocomplex within kidney excretion size range and eventually induces the nephrotoxicity. This study presents an approach to take advantage of the “weakness” of such unique interaction between AmB and albumin to form AmB nanocomplex beyond the size range of kidney excretion. Herein, a novel strategy was developed by directly assembling molecular BSA into larger-sized nanostructures with the reconstructed intermolecular disulfide bond and hydrophobic interaction. The rich binding sites of AmB within BSA nanostructures enabled the efficient AmB loading and forming nanoparticle (AmB-NP) which exceeds the size range of kidney excretion (~ 60 nm). We found nanoassembly with BSA redirected biodistribution of AmB with a 2.8-fold reduction of drug accumulation in the kidney and significantly improved its renal impairment in mice. Furthermore, we found that nanoassembly with BSA significantly increased the biodistribution of AmB in brain and endowed it 100-folds increase in pharmacological effect against meningoencephalitis caused by common fungal pathogen Cryptococcus neoformans . Together, this study not merely overcomes the nephrotoxicity of AmB using its “weakness” by a nanoassembly method, and provides a new strategy for reducing toxicity of drugs with high albumin binding rate in vivo .
研究领域:
药理学
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纳米医学
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传染病学
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产品关联
DOI
PubMed
高影响因子
Microbiology Spectrum
·
2023
·Vol. 11
·期 3
·
IF 3.7
Jinchao Xing,Chen Hu,Siqi Che,Yixin Lan,Lihong Huang,Lele Liu,Youqin Yin,Huanan Li,Ming Liao,Wenbao Qi
Japanese encephalitis virus (JEV) is a typical mosquito-borne flavivirus that can cause central nervous system diseases in humans and animals. Host factors attempt to limit virus replication when the viruses invade the host by using various strategies for replication. It is essential to clarify the host factors that affect the life cycle of JEV and explore its underlying mechanism. Here, we found that USP1-associated factor 1 (UAF1; also known as WD repeat-containing protein 48) modulated JEV replication. We found that JEV propagation significantly increased in UAF1-depleted Huh7 cells. Moreover, we found that knockdown of UAF1 activated cell autophagic flux in further functional analysis. Subsequently, we demonstrated that autophagy can be induced by JEV, which promotes viral replication by inhibiting interferon-stimulated gene (ISG) expression in Huh7 cells. The knockdown of UAF1 reduced ISG expression during JEV infection. To explore the possible roles of autophagy in UAF1-mediated inhibition of JEV propagation, we knocked out ATG7 to generate autophagy-deficient cells and found that depletion of UAF1 failed to promote JEV replication in ATG7 knockout cells. Moreover, in ATG7-deficient Huh7 cells, interference with UAF1 expression did not lead to the induction of autophagy. Taken together, these findings indicate that UAF1 is a critical regulator of autophagy and reveal a mechanism by which UAF1 knockdown activates autophagy to promote JEV replication.IMPORTANCE Host factors play an essential role in virus replication and pathogenesis. Although UAF1 is well known to form complexes with ubiquitin-specific proteases, little is known about the function of the UAF1 protein itself. In this study, we confirmed that UAF1 is involved in JEV replication. Notably, we discovered a novel function for UAF1 in regulating autophagy. Furthermore, we demonstrated that UAF1 modulated JEV replication through its autophagy regulation. This study is the first description of the novel function of UAF1 in regulating autophagy, and it clarifies the underlying mechanism of the antiviral effect of UAF1 against JEV. These results provide a new mechanistic insight into the functional annotation of UAF1 and provide a potential target for increasing virus production during vaccine production.
研究领域:
病毒学
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分子生物学
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细胞生物学
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传染病学
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产品关联
DOI
PubMed
高影响因子
VETERINARY MICROBIOLOGY
·
2025
·
IF 2.7
Qing Yang,Shengda Xie,Yundi Zhao,Xinxin Lin,Ning Wei,Miaolei Shi,Ruibing Cao
Japanese encephalitis virus (JEV) is a zoonotic pathogen that can be transmitted to humans and animals via arthropods, causing viral encephalitis. In this study, we investigated the role of transferrin receptor 1 (TfR1) in JEV infection. We found that knocking down TfR1 expression in A549 and HeLa cells significantly inhibited JEV entry, while overexpression of TfR1 in 293 T cells enhanced viral entry. The JEV E protein interacts with TfR1, specifically via the protease-like domain (residues 384–606). Additionally, the hTfR1 soluble ectodomain protein significantly blocked JEV infection in HeLa cells, and ferric ammonium citrate (FAC), an iron supplement, downregulated TfR1 expression and effectively inhibited JEV entry and infection. These findings identify TfR1 as an entry factor for JEV and a potential antiviral target, suggesting that small molecule inhibitors like FAC could offer a promising antiviral strategy.
研究领域:
病毒学
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分子生物学
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免疫学
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传染病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ANALYTICAL CHEMISTRY
·
2025
·
IF 6.7
Wanru Tian,Xin Zhao,Yao Li,Xuan Cheng,Zheng Yang,Peisen Zhang,Mingxia Jiao,Xiliang Luo
Encephalitis, a severe inflammatory brain condition, poses significant diagnostic challenges due to its heterogeneous symptoms and the limitations of conventional imaging techniques, such as magnetic resonance imaging (MRI), which often fail to detect early or subtle lesions. To address this clinical need, herein, a near-infrared (NIR) optical imaging strategy using engineered silver indium selenide quantum dots (QDs) was developed for precise and early detection of microencephalitic lesions. The QDs were synthesized via a robust aqueous-phase method with optimized NIR emission intensity through suppression of nonradiative recombination pathways. Surface modification with carboxyl-terminated poly(ethylene glycol) (carboxyl-PEG) enhanced colloidal stability, biocompatibility, and selective uptake capabilities by disease-associated M1 macrophages, improving localization at inflammatory sites. In vivo studies demonstrated the outstanding imaging performance of QDs, with encephalitis lesions clearly delineated at ultrahigh spatial resolution, enabling reliable detection of microinflammatory foci as small as 4.6 mm × 5.3 mm. This breakthrough capability facilitates early diagnosis by resolving sub-5 mm lesions, surpassing the sensitivity and resolution of conventional methods for the first time. By providing a noninvasive, high-resolution diagnostic tool, this technology holds potential for improving clinical decision-making and patient outcomes in encephalitis and other neuroinflammatory disorders, particularly in resource-limited settings where early diagnosis remains challenging.
研究领域:
神经免疫学
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分子影像学
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纳米医学
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转化医学
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生物材料
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神经病学
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炎症生物学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2023
·
IF 8.9
Dongxu Wang,Kai Yin,Yue Zhang,Hongmin Lu,Lulu Hou,Hongjing Zhao,Mingwei Xing
Endemic fluorosis (EF) has been listed as one of the serious public health problems in many countries. Long-term exposure to high fluoride can lead to severe neuropathological damage to the brain. Although long-term research has revealed the mechanism of some brain inflammation caused by excessive fluoride, the role of intercellular interactions, especially immune cells, in brain damage is still unclear. Fluoride can induce ferroptosis and inflammation in the brain in our study. A co-culture system of neutrophil extranets and primary neuronal cells showed that fluoride can aggravate neuronal cell inflammation by causing neutrophil extranets (NETs). In terms of the mechanism of action, we found that fluoride leads to the opening of calcium ion channels by causing neutrophil calcium imbalance, which in turn leads to the opening of L-type calcium ion channels (LTCC). Extracellular free iron enters the cell from the open LTCC, leading to neutrophil ferroptosis, which releases NETs. Blocking LTCC (nifedipine) rescued neutrophil ferroptosis and reduced the generation of NETs. Inhibition of ferroptosis (Fer-1) did not block cellular calcium imbalance. In summary, our study explores the role of NETs in fluoride-induced brain inflammation and suggests that blocking calcium channels may be one of the possibilities to rescue fluoride-induced ferroptosis.
研究领域:
神经科学
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免疫学
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毒理学
·
细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Ziwei Huang,Shan Li,Lishan Zhong,Yuan Su,Menghe Li,Xiaohui Wang,Zexu Wang,Zhiping Wang,Cuifang Ye,Zhe Ren,Xiao Wang,Qiongzhen Zeng,Kai Zheng,Yifei Wang
Background Herpes simplex virus type 1 (HSV-1)-induced herpes simplex encephalitis (HSE) has a high mortality rate in clinically immunocompromised patients, while recovered patients often experience neurological sequelae due to neuroinflammation. Nucleoside drugs and nucleoside analogues such as acyclovir and ganciclovir are mainly used in clinical treatment, and the emergence of resistant viral strains makes the development of new anti-herpesvirus encephalitis drugs urgent. Resveratrol is a multifunctional, plant-derived bioactive compound and its antiviral potential is attracting much attention. Purpose This study aimed to investigate the anti-HSV-1 mechanism of resveratrol in microglial cells and in the HSE mouse model. Methods The antiviral effect of resveratrol on HSV-1 infection was investigated by plaque assay, virus titer, immunofluorescence, Western blot and time-of-addition assay. The influence of resveratrol on stimulator of interferon gene (STING)/Nuclear Factor kappa B (NF-κB) signaling pathway-mediated neuroinflammation was examined by Western blot, RT-qPCR and ELISA. The interaction between resveratrol and STING/heat shock protein 90 beta (HSP90β) was evaluated by molecular modeling, co-immunoprecipitation, and drug affinity responsive target stability assay. The therapeutic effect of resveratrol on HSE was evaluated in the HSE mouse model by analyzing weight loss, neurodegenerative symptoms and histopathological scores. Results Resveratrol inhibited the early process of HSV-1 infection, and interfered with the STING/NF-κB signaling pathway to attenuate HSV-1-induced neuroinflammation and microglial M1 polarization, independent of its classical target Sirtuin1. Mechanistically, resveratrol completely bound to Glu515 and Lys491 of HSP90β, thus disrupting the HSP90β-STING interaction and promoting STING degradation. Resveratrol also significantly alleviated viral encephalitis and neuroinflammation caused by HSV-1 in the HSE mouse model. Conclusion Resveratrol acted as a non-classical HSP90β inhibitor, binding to the STING-HSP90β interaction site to promote STING degradation and attenuate HSV-1-induced encephalitis and neuroinflammation. These findings suggest the alternative strategy of targeting HSP90β and resveratrol-mediated inhibition of HSP90β as a potential antiviral approach.
研究领域:
病毒学
·
神经科学
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药理学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）