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- Enzyme activity of Aspergillus section Nigri strains isolated from the Korean fermentation starter, nuruk
- Eunji Jeong , Jeong-Ah Seo
- J. Microbiol. 2022;60(10):998-1006. Published online August 19, 2022
- DOI: https://doi.org/10.1007/s12275-022-2071-6
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- 1 Web of Science
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Abstract
- Aspergillus section Nigri is a fungus used industrially because of its ability to produce enzymes such as cellulolytic, amylolytic and proteolytic enzymes. In this study, we obtained twentyeight strains of Aspergillus section Nigri from the traditional Korean fermentation starter, nuruk, which is known as a mixed culture of enzymatic filamentous fungi and yeasts. All strains were identified as Aspergillus section Nigri through combined phylogenetic analysis using partial β-tubulin and calmodulin gene sequences. The cellulase, amylase and protease activities of Korean strains were measured and compared with ten reference strains of Aspergillus niger. Most Korean strains showed higher cellulolytic activity than reference strains, and Aspergillus neoniger KCN5 showed the highest β-glucosidase activity. Two-thirds of the Korean strains showed similar levels of α- and glucoamylase activity as the reference strains. The protease activity of Aspergillus section Nigri strains was the highest at pH 3.0, and A. niger KSJ2 showed the highest acidic protease activity. By comparing ten reference strains and twenty-eight Korean strains, our results suggested useful Aspergillus section Nigri strains from nuruk with high enzyme activity, such as KCN5 and KSJ2, and their potential for industrial applications as enzyme producers.
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- Effect of Aspergillus niger Fermentation on the Metabolites in Corn Stalks
Zhen Fan, Tianming Chen, Guolin Cai, Xiaoyu Huang, Suchuan Zhong, Xiaoming Li, Enping Zhang
Fermentation.2023; 9(1): 50. CrossRef
- Effect of Aspergillus niger Fermentation on the Metabolites in Corn Stalks
- Hepatitis C virus infection stimulates transforming growth factor-β1 expression through up-regulating miR-192
- Ji Hyun Kim , Chang Ho Lee , Seong-Wook Lee
- J. Microbiol. 2016;54(7):520-526. Published online June 28, 2016
- DOI: https://doi.org/10.1007/s12275-016-6240-3
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- 22 Crossref
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Abstract
- The objective of this study was to determine the molecular mechanisms underlying chronic liver injury and fibrosis caused by hepatitis C virus (HCV). This study revealed that miR-192 expression was induced by HCV infection without affecting viral replication. However, viral-induced miR-192 up-regulated transforming growth factor-β1 (TGF-β1) expression in liver cells at transcriptional level. TGF-β1 stimulation by HCV-induced miR-192 was caused through ZEB1 down-regulation and TGF-β1 increased miR-192 level via positive feedback pathway. Increase in miR-192 expression by HCV infection was due to HCV core protein released and/or expressed by viral infection. TGF-β1 promoter activity was also increased by HCV core protein in liver cells. Taken together, HCV infection resulted in increased TGF-β1 transcription in hepatocytes through ZEB1 down-regulation by HCV core-mediated miR-192 stimulation. Importantly, miR-192 inhibition with anti-miR-192 rescued ZEB1 expression down-regulated by HCV infection, thus reducing the level of TGF-β1 expression increased by HCV infection in hepatocytes. These results suggest a novel mechanism of HCV-mediated liver fibrogenesis with miR-192 being a potential molecular target to ameliorate viral pathogenesis.
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Citations
Citations to this article as recorded by- Hepatitis C Virus—Core Antigen: Implications in Diagnostic, Treatment Monitoring and Clinical Outcomes
Duong Hoang Huy Le, Sitthichai Kanokudom, Ha Minh Nguyen, Ritthideach Yorsaeng, Sittisak Honsawek, Sompong Vongpunsawad, Yong Poovorawan
Viruses.2024; 16(12): 1863. CrossRef - Hepatocytes infected with hepatitis C virus change immunological features in the liver microenvironment
Soo-Jeung Park, Young S. Hahn
Clinical and Molecular Hepatology.2023; 29(1): 65. CrossRef - Cancer Stem Cell and Hepatic Stellate Cells in Hepatocellular Carcinoma
Adriana G. Quiroz Reyes, Sonia A. Lozano Sepulveda, Natalia Martinez-Acuña, Jose F. Islas, Paulina Delgado Gonzalez, Tania Guadalupe Heredia Torres, Jorge Roacho Perez, Elsa N. Garza Treviño
Technology in Cancer Research & Treatment.2023;[Epub] CrossRef - Circulating miRNA-192 and miR-29a as Disease Progression Biomarkers in Hepatitis C Patients with a Prevalence of HCV Genotype 3
Amin Ullah, Irshad Ur Rehman, Katharina Ommer, Nadeem Ahmed, Margarete Odenthal, Xiaojie Yu, Jamshaid Ahmad, Tariq Nadeem, Qurban Ali, Bashir Ahmad
Genes.2023; 14(5): 1056. CrossRef - Rotavirus-Mediated Suppression of miRNA-192 Family and miRNA-181a Activates Wnt/β-Catenin Signaling Pathway: An In Vitro Study
Anwesha Banerjee, Mamta Chawla-Sarkar, Anupam Mukherjee
Viruses.2022; 14(3): 558. CrossRef - Roles of microRNAs in Hepatitis C Virus Replication and Pathogenesis
Hui-Chun Li, Chee-Hing Yang, Shih-Yen Lo
Viruses.2022; 14(8): 1776. CrossRef - ZEB1 serves an oncogenic role in the tumourigenesis of HCC by promoting cell proliferation, migration, and inhibiting apoptosis via Wnt/β-catenin signaling pathway
Liang-yun Li, Jun-fa Yang, Fan Rong, Zhi-pan Luo, Shuang Hu, Hui Fang, Ying Wu, Rui Yao, Wei-hao Kong, Xiao-wen Feng, Bang-jie Chen, Jun Li, Tao Xu
Acta Pharmacologica Sinica.2021; 42(10): 1676. CrossRef - miRNA expression profiles in liver grafts of HCV and HIV/HCV‐infected recipients, 6 months after liver transplantation
Michela Bulfoni, Riccardo Pravisani, Emiliano Dalla, Daniela Cesselli, Masaaki Hidaka, Carla Di Loreto, Susumu Eguchi, Umberto Baccarani
Journal of Medical Virology.2021; 93(8): 4992. CrossRef - Complexation with Random Methyl-β-Cyclodextrin and (2-Hidroxypropyl)-β-Cyclodextrin Enhances In Vivo Anti-Fibrotic and Anti-Inflammatory Effects of Chrysin via the Inhibition of NF-κB and TGF-β1/Smad Signaling Pathways and Modulation of Hepatic Pro/Anti-F
Alina Ciceu, Cornel Balta, Hidegard Herman, Sami Gharbia, Simona-Rebeca Ignat, Sorina Dinescu, Judit Váradi, Ferenc Fenyvesi, Szilvia Gyöngyösi, Anca Hermenean, Marieta Costache
International Journal of Molecular Sciences.2021; 22(4): 1869. CrossRef - HCV Proteins Modulate the Host Cell miRNA Expression Contributing to Hepatitis C Pathogenesis and Hepatocellular Carcinoma Development
Devis Pascut, Minh Hoang, Nhu N. Q. Nguyen, Muhammad Yogi Pratama, Claudio Tiribelli
Cancers.2021; 13(10): 2485. CrossRef -
Cell‐to‐cell spread of vaccinia virus is promoted by
TGF
‐β‐independent Smad4 signalling
Anjali Gowripalan, Caitlin R. Abbott, Christopher McKenzie, Weng S. Chan, Gunasegaran Karupiah, Laurence Levy, Timothy P. Newsome
Cellular Microbiology.2020;[Epub] CrossRef - Exosomal miRNAs: Novel Players in Viral Infection
Javid Sadri Nahand, Maryam Mahjoubin-Tehran, Mohsen Moghoofei, Mohammad Hossein Pourhanifeh, Hamid Reza Mirzaei, Zatollah Asemi, Alireza Khatami, Farah Bokharaei-Salim, Hamed Mirzaei, Michael R Hamblin
Epigenomics.2020; 12(4): 353. CrossRef - Tumor necrosis family receptor superfamily member 9/tumor necrosis factor receptor-associated factor 1 pathway on hepatitis C viral persistence and natural history
Julia Peña-Asensio, Eduardo Sanz-de-Villalobos, Joaquín Miquel, Juan Ramón Larrubia
World Journal of Hepatology.2020; 12(10): 754. CrossRef - Role of non-coding RNAs in liver disease progression to hepatocellular carcinoma
Mi Jeong Heo, Jessica Yun, Sang Geon Kim
Archives of Pharmacal Research.2019; 42(1): 48. CrossRef - Mechanisms Underlying Hepatitis C Virus-Associated Hepatic Fibrosis
Mousumi Khatun, Ratna B. Ray
Cells.2019; 8(10): 1249. CrossRef - ZEB1 regulates the activation of hepatic stellate cells through Wnt/β-catenin signaling pathway
Liang-yun Li, Chen-chen Yang, Jun-fa Yang, Hao-dong Li, Bo-yu Zhang, Hong Zhou, Shuang Hu, Kun Wang, Cheng Huang, Xiao-ming Meng, Huan Zhou, Lei Zhang, Jun Li, Tao Xu
European Journal of Pharmacology.2019; 865: 172787. CrossRef - microRNAs as therapeutic targets in intestinal diseases
Chen Wang, Jiangning Chen
ExRNA.2019;[Epub] CrossRef - miRNAs regulate immune response and signaling during hepatitis C virus infection
Huange Zhu, Yan Geng, Qian He, Miaoxian Li
European Journal of Medical Research.2018;[Epub] CrossRef - Exendin-4 ameliorates high glucose-induced fibrosis by inhibiting the secretion of miR-192 from injured renal tubular epithelial cells
Yijie Jia, Zongji Zheng, Meiping Guan, Qian Zhang, Yang Li, Ling Wang, Yaoming Xue
Experimental & Molecular Medicine.2018; 50(5): 1. CrossRef - Dysregulation of cellular microRNAs by human oncogenic viruses – Implications for tumorigenesis
Joana M.O. Santos, Rui M. Gil da Costa, Rui Medeiros
Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms.2018; 1861(2): 95. CrossRef -
According to Hepatitis C Virus (HCV) Infection Stage, Interleukin-7 Plus 4-1BB Triggering Alone or Combined with PD-1 Blockade Increases TRAF1
low
HCV-Specific CD8
+
Cell Reactivity
Elia Moreno-Cubero, Dolores Subirá, Eduardo Sanz-de-Villalobos, Trinidad Parra-Cid, Antonio Madejón, Joaquín Miquel, Antonio Olveira, Alejandro González-Praetorius, Javier García-Samaniego, Juan-Ramón Larrubia, Michael S. Diamond
Journal of Virology.2018;[Epub] CrossRef - Hepatitis C virus–induced tumor‐initiating cancer stem–like cells activate stromal fibroblasts in a xenograft tumor model
Reina Sasaki, Pradip Devhare, Ratna B. Ray, Ranjit Ray
Hepatology.2017; 66(6): 1766. CrossRef
- Hepatitis C Virus—Core Antigen: Implications in Diagnostic, Treatment Monitoring and Clinical Outcomes
- Roles of human apolipoprotein E in the infectivity and replication of hepatitis C virus genotype 2a
- Bo-Kyoung Jung , Hye-Ran Kim , Gyu-Nam Park , Guangxiang Luo , Kyung-Soo Chang
- J. Microbiol. 2016;54(6):451-458. Published online May 27, 2016
- DOI: https://doi.org/10.1007/s12275-016-6099-3
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- 2 Crossref
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Abstract
- Hepatitis C virus (HCV) infection is associated with lipoproteins, and apolipoprotein E (apoE) plays an essential role in infectious HCV particles. Although the role of apoE in HCV infection is well known, its role in the replication of HCV remains unclear. The aims of this study were to determine the role of apoE in the RNA replication of major HCV genotypes 1b and 2a, and to determine whether this role is HCVgenotype- dependent using HCV genotype 1b replicon cells and HCV genotype 2a producing (HP) cells. HCV infection was blocked in Huh7.5 cells treated with low-density lipoproteins, very low-density lipoproteins, or apoE3. An apoE3- specific monoclonal antibody also efficiently neutralized HCV infectivity, and HCV infection was dramatically suppressed by the knockdown of apoE expression with an apoE-specific small interfering RNA, suggesting a requirement for apoE in infectious HCV particles. HCV RNA replication was not affected in HP cells treated with each apoE isoform or transfected with apoE-specific siRNAs. However, the knockdown of apoE expression suppressed RNA replication of HCV genotype 1b. The siRNA-mediated knockdown of apoE, apoA1, and apoB expression also suppressed the RNA replication of HCV genotype 1b, but not that of HCV genotype 2a. Taken together, these findings indicate that apoE plays an important role in HCV genotype 2a infection and in HCV genotype 1b RNA replication, but not in the replication of HCV genotype 2a. These results provide important information for the future development of HCV-genotypespecific anti-HCV agents.
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Citations
Citations to this article as recorded by
Review
- MINIREVIEW] The Role of MicroRNAs in Hepatitis C Virus Replication and Related Liver Diseases
- Chang Ho Lee , Ji Hyun Kim , Seong-Wook Lee
- J. Microbiol. 2014;52(6):445-451. Published online May 29, 2014
- DOI: https://doi.org/10.1007/s12275-014-4267-x
- 47 View
- 0 Download
- 32 Crossref
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Abstract
- Hepatitis C virus (HCV) infection is a worldwide health problem and is one of the main causes of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). However, only limited therapeutic options and no vaccines are currently available against HCV infection. Recent studies of microRNAs (miRNAs), which are able to regulate HCV replication and its related liver diseases by directly interacting with the HCV genome or indirectly controlling virus-associated host pathways, have broadened our understanding of the HCV life cycle. HCV utilizes host cellular miRNAs and modulates expression of miRNAs in infected hepatocytes for its infection and propagation. Moreover, such miRNAs directly or indirectly alter HCV replication efficiency and induce liver diseases including liver fibrosis, cirrhosis, or HCC. Representatively, miR-122 directly modulates the HCV life cycle by increasing HCV translation and genomic RNA stability. Recently, a phase IIa clinical trial with miravirsen, an LNA form of antimiR-122 oligonucleotides, showed significant reduction in serum HCV levels in patients chronically infected with HCV with no detectible evidence of resistance. In addition to miR-122, other miRNAs involved in the regulation of HCV propagation could be targeted in strategies to modulate HCV replication and pathogenesis. In this review, we summarize the features of miRNAs critical for HCV replication and HCV-mediated liver abnormalities and briefly discuss their potential application as therapeutic reagents for the treatment of HCV infection and its related diseases.
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Citations
Citations to this article as recorded by- MiR-130c-5p targets the SHVV n gene and upregulates immune cytokines (IL-6, IL-22, IL-1β) to inhibit viral replication
Jin Wei, Yan Ji, Yaqian Bai, Rui Cheng, Jiaqi Zhang, Xianqin Hu, Chi Zhang
Frontiers in Immunology.2024;[Epub] CrossRef - Research advances in serum chitinase-3-like protein 1 in liver fibrosis
Xingwei Hu, Wenhan Liu, Jianhua Liu, Bojian Wang, Xiaosong Qin
Frontiers in Medicine.2024;[Epub] CrossRef - A Review of miRNA Regulation in Japanese Encephalitis (JEV) Virus
Infection
Maneesh Kumar, Ganesh Chandra Sahoo, Vidya Nand Rabi Das, Kamal Singh, Krishna Pandey
Current Pharmaceutical Biotechnology.2024; 25(5): 521. CrossRef - Cold exposure impairs extracellular vesicle swarm–mediated nasal antiviral immunity
Di Huang, Maie S. Taha, Angela L. Nocera, Alan D. Workman, Mansoor M. Amiji, Benjamin S. Bleier
Journal of Allergy and Clinical Immunology.2023; 151(2): 509. CrossRef - Circulating miRNA-192 and miR-29a as Disease Progression Biomarkers in Hepatitis C Patients with a Prevalence of HCV Genotype 3
Amin Ullah, Irshad Ur Rehman, Katharina Ommer, Nadeem Ahmed, Margarete Odenthal, Xiaojie Yu, Jamshaid Ahmad, Tariq Nadeem, Qurban Ali, Bashir Ahmad
Genes.2023; 14(5): 1056. CrossRef - Hepatocellular carcinoma, hepatitis C virus infection and miRNA involvement: Perspectives for new therapeutic approaches
Ester Badami, Rosalia Busà, Bruno Douradinha, Giovanna Russelli, Vitale Miceli, Alessia Gallo, Giovanni Zito, Pier Giulio Conaldi, Gioacchin Iannolo
World Journal of Gastroenterology.2022; 28(22): 2417. CrossRef - Host Epigenetic Alterations and Hepatitis B Virus-Associated Hepatocellular Carcinoma
Mirjam B. Zeisel, Francesca Guerrieri, Massimo Levrero
Journal of Clinical Medicine.2021; 10(8): 1715. CrossRef - MiRNAs and Cancer: Key Link in Diagnosis and Therapy
Yu Shi, Zihao Liu, Qun Lin, Qing Luo, Yinghuan Cen, Juanmei Li, Xiaolin Fang, Chang Gong
Genes.2021; 12(8): 1289. CrossRef - Circulating microRNA-155 is associated with insulin resistance in chronic hepatitis C patients
Nourhan M. El Samaloty, Zeinab A. Hassan, Zeinab M. Hefny, Dalia H.A. Abdelaziz
Arab Journal of Gastroenterology.2019; 20(1): 1. CrossRef - Integrated Analysis of miRNA and mRNA Expression Profiles in Spleen of Specific Pathogen-Free Chicken Infected with Avian Reticuloendotheliosis Virus Strain SNV
Shuo Gao, Hao Jiang, Jie Sun, Youxiang Diao, Yi Tang, Jingdong Hu
International Journal of Molecular Sciences.2019; 20(5): 1041. CrossRef - Molecular mechanisms of circular RNAs, transforming growth factor‐β, and long noncoding RNAs in hepatocellular carcinoma
Wenkang Shang, Gabriel Komla Adzika, Yujie Li, Qike Huang, Ningding Ding, Bianca Chinembiri, Mohammad Sajjad Ibn Rashid, Jeremiah Ong'achwa Machuki
Cancer Medicine.2019; 8(15): 6684. CrossRef - MicroRNA Expression in Focal Nodular Hyperplasia in Comparison with Cirrhosis and Hepatocellular Carcinoma
Gábor Lendvai, Tímea Szekerczés, Benedek Gyöngyösi, Krisztina Schlachter, Endre Kontsek, Adrián Pesti, Attila Patonai, Klára Werling, Ilona Kovalszky, Zsuzsa Schaff, András Kiss
Pathology & Oncology Research.2019; 25(3): 1103. CrossRef - gga-miR-21 modulates Mycoplasma gallisepticum (HS strain)-Induced inflammation via targeting MAP3K1 and activating MAPKs and NF-κB pathways
Yabo Zhao, Mengyun Zou, Yingfei Sun, Kang Zhang, Xiuli Peng
Veterinary Microbiology.2019; 237: 108407. CrossRef - miR-27b-mediated suppression of aquaporin-11 expression in hepatocytes reduces HCV genomic RNA levels but not viral titers
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Cancers.2018; 10(8): 258. CrossRef - Upregulated microRNA-429 inhibits the migration of HCC cells by targeting TRAF6 through the NF-κB pathway
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Oncology Reports.2017; 37(5): 2883. CrossRef - Hepatitis C virus and atherosclerosis: A legacy after virologic cure?
M.F. Bassendine, S.U. Nielsen, S.H. Bridge, D.J. Felmlee, D.A. Sheridan, C.J. Packard, R.D. Neely
Clinics and Research in Hepatology and Gastroenterology.2017; 41(1): 25. CrossRef - The Potential of MicroRNAs as Novel Biomarkers for Transplant Rejection
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Journal of Immunology Research.2017; 2017: 1. CrossRef - The notorious R.N.A. in the spotlight - drug or target for the treatment of disease
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RNA Biology.2017; 14(5): 651. CrossRef - Decline of miR‐124 in myeloid cells promotes regulatory T‐cell development in hepatitis C virus infection
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Immunology.2017; 150(2): 213. CrossRef - Protection of CD4+ T cells from hepatitis C virus infection-associated senescence via ΔNp63–miR-181a–Sirt1 pathway
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Journal of Leukocyte Biology.2016; 100(5): 1201. CrossRef - Achieving sustained virologic response after interferon‐free hepatitis C virus treatment correlates with hepatic interferon gene expression changes independent of cirrhosis
E. G. Meissner, A. Kohli, K. Virtaneva, D. Sturdevant, C. Martens, S. F. Porcella, J. G. McHutchison, H. Masur, S. Kottilil
Journal of Viral Hepatitis.2016; 23(7): 496. CrossRef - MicroRNA-mediated interactions between host and hepatitis C virus
Hu Li
World Journal of Gastroenterology.2016; 22(4): 1487. CrossRef - Hepatitis C virus infection stimulates transforming growth factor-β1 expression through up-regulating miR-192
Ji Hyun Kim, Chang Ho Lee, Seong-Wook Lee
Journal of Microbiology.2016; 54(7): 520. CrossRef - MicroRNA-33a-5p Modulates Japanese Encephalitis Virus Replication by Targeting Eukaryotic Translation Elongation Factor 1A1
Zheng Chen, Jing Ye, Usama Ashraf, Yunchuan Li, Siqi Wei, Shengfeng Wan, Ali Zohaib, Yunfeng Song, Huanchun Chen, Shengbo Cao, R. M. Sandri-Goldin
Journal of Virology.2016; 90(7): 3722. CrossRef - Circulating MiRNA-122 Levels Are Associated with Hepatic Necroinflammation and Portal Hypertension in HIV/HCV Coinfection
Christian Jansen, Thomas Reiberger, Jia Huang, Hannah Eischeid, Robert Schierwagen, Mattias Mandorfer, Evrim Anadol, Philipp Schwabl, Carolynne Schwarze-Zander, Ute Warnecke-Eberz, Christian P. Strassburg, Jürgen K. Rockstroh, Markus Peck-Radosavljevic, M
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M Battistella, PA Marsden
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Jason Lamontagne
World Journal of Gastroenterology.2015; 21(24): 7375. CrossRef - Hepatitis C virus–induced reduction in miR‐181a impairs CD4+ T‐cell responses through overexpression of DUSP6
Guang Y. Li, Yun Zhou, Ruo S. Ying, Lei Shi, Yong Q. Cheng, Jun P. Ren, Jeddidiah W.D. Griffin, Zhan S. Jia, Chuan F. Li, Jonathan P. Moorman, Zhi Q. Yao
Hepatology.2015; 61(4): 1163. CrossRef - miR-141 targets ZEB2 to suppress HCC progression
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Tumor Biology.2014; 35(10): 9993. CrossRef
- MiR-130c-5p targets the SHVV n gene and upregulates immune cytokines (IL-6, IL-22, IL-1β) to inhibit viral replication
Research Support, Non-U.S. Gov't
- Application of Bovine Viral Diarrhoea Virus as an Internal Control in Nucleic Acid Amplification Tests for Hepatitis C Virus RNA in Plasma-Derived Products
- Si Hyung Yoo , Seung Hee Hong , Sa Rah Jung , Su Jin Park , Nam Kyung Lee , Soon Nam Kim , Sang Mo Kang , Hong Ki Min , Sue Nie Park , Seung Hwa Hong
- J. Microbiol. 2006;44(1):72-76.
- DOI: https://doi.org/2334 [pii]
- 37 View
- 0 Download
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Abstract
- Plasma-derived products are produced from plasma via fractionation and chromatography techniques, but can also be produced by other methods. In the performance of nucleic acid amplification tests (NAT) with plasma-derived products, it is necessary to include an internal control for the monitoring of all procedures. In order to avoid false negative results, we confirmed the usefulness of the bovine viral diarrhoea virus (BVDV) for use as an internal control in the detection of hepatitis C virus (HCV) RNA in plasma-derived products. These products, which were spiked with BVDV, were extracted and then NAT was performed. Specificity and sensitivity were determined via the adjustment of primer concentrations and annealing temperatures. BVDV detection allows for validation in the extraction, reverse transcription, and amplification techniques used for HCV detection in plasma-derived products.
Journal Article
- Hepatitis C Virus Non-structural Protein NS4B Can Modulate an Unfolded Protein Response
- Yi Zheng , Bo Gao , Li Ye , Lingbao Kong , Wei Jing , Xiaojun Yang , Zhenghui Wu , Linbai Ye
- J. Microbiol. 2005;43(6):529-536.
- DOI: https://doi.org/2294 [pii]
- 37 View
- 0 Download
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Abstract
- Viral infection causes stress to the endoplasmic reticulum (ER). The response to endoplasmic reticulum stress, known as the unfolded protein response (UPR), is designed to eliminate misfolded proteins and allow the cell to recover. The role of hepatitis C virus (HCV) non-structural protein NS4B, a component of the HCV replicons that induce UPR, is incompletely understood. We demonstrate that HCV NS4B could induce activating transcription factor (ATF6) and inositol-requiring enzyme 1 (IRE1), to favor the HCV subreplicon and HCV viral replication. HCV NS4B activated the IRE1 pathway, as indicated by splicing of X box-binding protein (Xbp-1) mRNA. However, transcriptional activation of the XBP-1 target gene, EDEM (ER degradation-enhancing a-mannosidase-like protein, a protein degradation factor), was inhibited. These results imply that NS4B might induce UPR through ATF6 and IRE1-XBP1 pathways, but might also modify the outcome to benefit HCV or HCV subreplicon replication.
Research Support, Non-U.S. Gov't
- Hepatitis C Virus (HCV) Genotyping by Annealing Reverse Transcription-PCR Products with Genotype-Specific Capture Probes
- Jungmin Rho , Jong Soon Ryu , Wonhee Hur , Chang Wook Kim , Jeong Won Jang , Si Hyun Bae , Jong Young Choi , Sung Key Jang , Seung Kew Yoon
- J. Microbiol. 2008;46(1):81-87.
- DOI: https://doi.org/10.1007/s12275-007-0121-8
- 38 View
- 0 Download
- 18 Scopus
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Abstract
- The genotype of the hepatitis C virus (HCV) strain infecting a given patient is an important predictive factor for the clinical outcome of chronic liver disease and its response to anti-viral therapeutic agents. We herein sought to develop a new easy, sensitive and accurate HCV genotyping method using annealing genotype- specific capture probes (AGSCP) in an automation-friendly 96-well plate format. The validation of our new AGSCP was performed using the Standard HCV Genotype Panel. We then used both our AGSCP and the commercially available INNO-LiPA assay to analyze the HCV genotypes from 111 Korean patients. Discordant results were analyzed by direct sequencing. AGSCP successfully genotyped the standard panel. The genotypes of 111 patient samples were also obtained successfully by AGSCP and INNO-LiPA. We observed a high concordance rate (93 matched samples, 83.8%) between the two assays. Sequencing analysis of the 18 discordant results revealed that the AGSCP had correctly identified 12 samples, whereas the INNO- LiPA had correctly identified only 6. These results collectively indicate that AGSCP assay is a convenient and sensitive method for large-scale genotyping, and it may be a promising tool for the determination of HCV and other genotypes in clinical settings.
- Hepatitis C Virus Core Protein Sensitizes Cells to Apoptosis Induced by Anti-Cancer Drug
- Kang, Mun Il , Cho, Mong , Kim, Sun Hee , Kang, Chi Dug , Kim, Dong Wan
- J. Microbiol. 1999;37(2):90-96.
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Abstract
- The core protein of the hepatitis C virus (HCV) is a multifunctional protein. The HCV core protein was reported to regulate cellular gene expression and transform primary rat embryo fibroblast cells. However, the role of the core protein in the pathogenesis of HCV-associated liver diseases is not well understood. To investigate the functional role of the core protein in cytophathogenicity, we have constructed stable expression systems of full length or truncated HCV core protein lacking the C-terminal hyderophobic domains and established HepG2 cell clones constitutively expressing the core protein. The full length core protein was localized in the cytoplasm and the C-terminal truncated core protein was localized in the nucleus. HepG2 cells expressing nuclear, truncated core protein showed elevated cell death during cultivation compared to untransfected cells and full length core-expressing cells. In the treatment with bleomycin, both cell clones expressing full length or truncated core protein appeared to be more sensitive to bleomycin than the parental HepG2 cells. These results suggest that the core protein may play a role in HCV pathogenesis promoting apoptotic cell death of infected cells.
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