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herpes simplex virus-1 infection or Simian virus 40-mediated immortalization of corneal cells causes permanent translocation of NLRP3 to the nuclei

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International Journal of Ophthalmology(English edition) 2015年第1期8卷 46-51页

作者： Shu-Long Wang Ge Zhao Wei Zhu Xiao-Meng Dong Ting Liu Yuan-Yuan Li Wen-Gang Song Yi-Qiang Wang Department of Immunology Taishan Medical University Shandong Provincial Key Laboratory of Ophthalmology Shandong Eye Institute Department of Immunology Qingdao University MOH Key Lab of Thrombosis and Hemostasis Jiangsu Institute of Hematology the First Affiliated Hospital of Soochow University

AIM: To investigate into the potential involvement of pyrin containing 3 gene(NLRP3), a member of the nucleotide-binding oligomerization domain-like receptors with cytosolic pattern recognition, in the host defense of corneas against ***: The herpes viral keratitis model was utilized in BALB/c mice with inoculation of herpes simplex virus-1(HSV-1). Corneal tissues removed during therapy of patients with viral keratitis as well as a Simian vacuolating virus 40(SV40)-immortalized human corneal epithelial cell line were also *** was used to detect NLRP3 in these subjects, focusing on their distribution in tissue or cells. Western blot was used to measure the level of NLRP3 and another two related molecules in NLPR3 inflammasome, namely caspase-1 and IL-1β.RESULTS: The NLRP3 activation induced by HSV-1infection in corneas was accompanied with redistribution of NLRP3 from the cytoplasm to the nucleus in both murine and human corneal epithelial cells. Furthermore,in the SV40-immortalized human corneal epithelial cells,NLRP3 was exclusively located in the nucleus, and treatment of the cells with high concentration of extracellular potassium(known as an inhibitor of NLRP3activation) effectively drove NLRP3 back to the cytoplasm as reflected by both immunohistochemistry and Western blot.· CONCLUSION: It is proposed that herpes virus infection activates and causes redistribution of NLRP3 to nuclei. Whether this NLRP3 translocation occurs with other viral infections and in other cell types merit further study.

关键词： pyrin containing 3 gene inflammasome translocation herpes simplex virus-1 keratitis human corneal epithelial cell Simian vacuolating virus 40 immortalization

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Inhibitory Effects of Ginsenoside Rb1 on Apoptosis Caused by HSV-1 in Human Glioma Cells

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Virologica Sinica 2012年第1期27卷 19-25页

作者： Yuan-Yuan Liang Bin Wang Dong-Meng Qian Ling Li Zhi-Hao Wang Ming Hu Xu-Xia Song Department of Microbiology Key Laboratory of Medicine and Biotechnology of QingdaoQingdao UniversityQingdao 266071ShandongChina

To investigate the inhibitory effects of Ginsenoside Rbl （GRbl） on apoptosis caused by herpes simplex virus-1 （HSV-1） in Human Glioma Cells （U251）, U251 cells were infected by HSV-1 at a multiplicity of infection of 5 and GRbl, GRbl＋HSV-1, HSV-1 and control groups. MTT and cell apoptosis assays were used to detect the inhibitory effects of GRbl on the apoptosis of U251 cells that caused by HSV-1 infection for various concentrations of drug and virus treatments by MTT assay. We found that in the 400 μg/mL GRb 1 and 400 μg/mL GRbl＋HSV-1 groups, MTT values were higher than control group at all times （P〈0.05）. Moreover, the apoptosis rate in the 400 μg/mL GRbl＋HSV-1 group was lower than the HSV-1 group （P〈0. 05）. These results confirmed that, at appropriate concentrations, GRbl could inhibit nerve cell apoptosis in HSV-1 infections.

关键词： Ginsenoside Rb 1 herpes simplex virus-1 Human Glioma Cells Apoptosis

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Bioinformatics Review of the Role of HSV-1 in Alzheimer’s Disease

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Advances in Alzheimer's Disease 2020年第3期9卷 57-75页

作者： Brian T. Reiss Meade C. Eggleston Arah C. Godbole Julia A. Marut Cecelia M. McCann Jessica A. Cottrell Tinchun Chu Sulie L. Chang Department of Biological Sciences Seton Hall University South Orange NJ USA Institute of Neuroimmune Pharmacology Seton Hall University South Orange NJ USA

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the progressive loss of cognitive functions in affected individuals. Brain tissue pathology is associated with the formation of senile plaques which result from the over-production of amyloid β (Aβ), due to the cleavage of a membrane bound glycoprotein. It is unclear what causes AD and its associated pathologies, but age and genetic predisposition play an import role in the likelihood of disease development. Studies have shown that the reactivation of latent herpes simplex virus 1 (HSV-1) infection can lead to the neuropathy of acute herpes simplex encephalitis (HSE), which causes similar symptoms to AD. HSV-1 infection is a known risk factor for the development of AD, but no study has determined a definitive causal relationship. Using the Qiagen Ingenuity Pathway Analysis (IPA) tool, the inhibitory relationship between therapeutics for AD and HSV-1 were explored. Thirteen drugs developed to decrease Aβ buildup in AD and 32 drugs that act as HSV antivirals were retrieved from the data in the Qiagen Knowledge Base. These drugs were analyzed displayed as two separate networks. While many promising Aβ aggregation-targeting drugs have been discontinued due to lack of efficacy, HSV drugs could serve as potential therapeutics for those with AD. This review aims to describe new insights on how HSV-1 relates to the development of AD and highlight the mechanism of action of Aβ

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HISP-1 Inhibits HSV-1 Infection in Cultured Vero Cells

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Advances in Bioscience and Biotechnology 2024年第4期15卷 269-288页

作者： Sandra D. Adams Kevin T. Bilyk Modukuri V. Ramani Gottumukkala V. Subbaraju Department of Biology Montclair State University Montclair USA Department of Chemistry Andhara University Visakhapatnam India

herpes simplex virus-1 (HSV-1) remains a leading cause of viral disease worldwide and is spread by direct contact with infected lesions. There is no vaccine against HSV-1 infections and there remains a need to identify therapeutics that could reduce the spread. In this study various hispolon compounds were analyzed to determine their antiviral potential against HSV-1 infections in cultured Vero cells. To determine the effects on infectivity and possible mechanisms of inhibition, the following assays were conducted. In vitro cytotoxicity assays were conducted to determine the effect of the compounds on cell viability and the maximum non-cytotoxic concentrations. Antiviral assays measured cell viability, percent inhibition of infection following treatment with the compounds, and the effect on the viral infection cycle. These effects were visualized using inverted light and fluorescent microscopy. Of the 24 hispolons tested, only hispolon pyrazole-1 (HISP-1) demonstrated antiviral effects. HISP-1 was demonstrated to effect early stages in HSV-1 infection in cultured Vero cells (attachment, penetration, and post-penetration). In silico modeling analyses were conducted to analyze the interactions between HISP-1 and viral glycoprotein D (gD). HISP-1 is safe at concentrations tested and is effective in inhibiting infection of HSV-1 in cultured cells. HISP-1 has potential for therapeutic use as an antiviral against HSV-1 infection, could work in synergy with other antivirals that work be a different modality, and could be developed as a component of a topical agent to reduce the spread of HSV-1 infections.

关键词： Hispolon herpes simplex virus-1 Antiviral Curcumin

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