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| 1 | Varicella-zoster virus ORF7 interacts with ORF53 and plays a role in its trans-Golgi network localization显示文摘Varicella-zoster virus(VZV) is a neurotropic alphaherpesvirus that causes chickenpox and shingles. ORF7 is an important virulence determinant of VZV in both human skin and nerve tissues,however, its specific function and involved molecular mechanism in VZV pathogenesis remain largely elusive. Previous yeast two-hybrid studies on intraviral protein-protein interaction network in herpesviruses have revealed that VZV ORF7 may interact with ORF53, which is a virtually unstudied but essential viral protein. The aim of this study is to identify and characterize VZV ORF53, and to investigate its relationship with ORF7. For this purpose, we prepared monoclonal antibodies against ORF53 and, for the first time, characterized it as a ~40 k Da viral protein predominantly localizing to the trans-Golgi network of the infected host cell. Next, we further confirmed the interaction between ORF7 and ORF53 by co-immunoprecipitation and co-localization studies in both plasmid-transfected and VZV-infected cells. Moreover, interestingly, we found that ORF53 lost its trans-Golgi network localization and became dispersed in the cytoplasm of host cells infected with an ORF7-deleted recombinant VZV, and thus ORF7 seems to play a role in normal subcellular localization of ORF53. Collectively, these results suggested that ORF7 and ORF53 may function as a complex during infection, which may be implicated in VZV pathogenesis. | Wei Wang Wenkun Fu Dequan Pan Linli Cai Jianghui Ye Jian Liu Che Liu Yuqiong Que Ningshao Xia Hua Zhu Tong Cheng | 2017 | Virologica Sinica2017，32，5： | 1 |
| 2 | In-situ oxidized tungsten disulfide nanosheets achieve ultrafast photocatalytic extraction of uranium through hydroxyl-mediated binding and reduction显示文摘Photoreduction of hexavalent uranium(U(VI))by semiconductor provides a novel and effective avenue for uranium extraction.Unfortunately,the traditional metal oxide and sulfide semiconductors suffer from the lack of confinement sites to U(VI),which resulted in the long period(~1 h)to achieve a high U(VI)extraction efficiency of>90%.Herein,we successfully constructed WS2 nanosheets and created in-situ oxidized domains on the surfaces(O-WS_(2))to promote the uranium extraction and the corresponding removal kinetics.In this system,the O_(7.7-)WS_(2) nanosheets exhibited a considerable U(VI)extraction efficiency of>90%within 20 min in 8 mg·L^(–1) U(VI)-containing solution,which represented the highly efficient U(VI)removal performance.In 200 mg·L^(–1) U(VI)-containing solution,the O7.7-WS2 nanosheets exhibited an extraction capacity of 652.4 mg·g^(-1).The mechanism study revealed that the oxidized surface tended to trap hydrogen atom and in-situ form hydroxyl groups in defect sites.Evidenced by a series of experiment,such as kinetic isotope effect,1H nuclear magnetic resonance(NMR)spectra,and X-ray absorption near-edge structure(XANES)spectra,the in-situ formed hydroxyl groups participated in the uranium reduction,which dramatically enhanced uranium extraction kinetics and efficiency. | Huanhuan Liu Jia Lei Changyao Gong Ye Li Huimei Chen Jiali Chen Fengchun Wen Dengjiang Fu Yan Liu Wenkun Zhu Rong He | 2022 | Nano Research2022，15，10： | 0 |
| 3 | Development of A Neonatal Mouse Model for Coxsackievirus B1 Antiviral Evaluation显示文摘Coxsackievirus B1(CVB1) is a leading causative agent of severe infectious diseases in humans and has been reported to be associated with outbreaks of aseptic meningitis, myocarditis, and the development of chronic diseases such as type 1 diabetes mellitus(T1DM). There is no approved vaccine or effective antiviral therapy to treat CBV1 infection. And animal models to assess the effects of antiviral agents and vaccine remain limited. In this study, we established a neonatal mouse model of CVB1 using a clinically isolated strain to characterize the pathological manifestations of virus infection and to promote the development of vaccines and antiviral drugs against CVB1. One-day-old BALB/c mice were susceptible to CVB1 infection by intraperitoneal injection. Mice challenged with CVB1 at a low dose [10 median tissue culture infective dose(TCID_(50))] exhibited a series of clinical symptoms, such as inactivity, emaciation, limb weakness, hair thinning,hunching and even death. Pathological examination and tissue viral load analysis showed that positive signals of CVB1 were detected in the heart, spinal cord, limb muscle and kidney without pathological damage. Particularly, CVB1 had a strong tropism towards the pancreas, causing severe cellular necrosis with inflammatory infiltration, and was spread by viraemia. Notably, the monoclonal antibody(mAb) 6H5 and antisera elicited from CVB1-vaccinated mice effectively protected the mice from CVB1 infection in the mouse model. In summary, the established neonatal mouse model is an effective tool for evaluating the efficacy of CVB1 antiviral reagents and vaccines. | Zhichao Yin Yuanyuan Wu Rui Zhu Longfa Xu Yu Lin Hongwei Yang Wenkun Fu Qiongzi Huang Dongqing Zhang Jue Wang Wei Wang Yingbin Wang Tong Cheng Ningshao Xia | 2021 | Virologica Sinica2021，36，6： | 0 |
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