FullText URL K0005289_other1.pdf
Author Takeda, Midori| Ikeda, Masanori| Ariumi, Yasuo| Wakita, Takaji| Kato, Nobuyuki|
Note 学位審査副論文
Published Date 2012-07
Publication Title Journal of General Virology
Volume volume93
Issue issue7
Publisher Cambridge Univ. Press for the Society for General Microbiology
Start Page 1422
End Page 1431
ISSN 0022-1317
NCID AA00698722
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version author
PubMed ID 22456614
DOI 10.1099/vir.0.040725-0
Web of Sience KeyUT 000306348900003
Related Url https://doi.org/10.1099/vir.0.040725-0 http://ousar.lib.okayama-u.ac.jp/54272
FullText URL K0005288_other.pdf
Author Sejima, Hiroe| Mori, Kyoko| Ariumi, Yasuo| Ikeda, Masanori| Kato, Nobuyuki|
Keywords HCV HCV RNA replication system Li23 cells Long-term RNA replication Upregulated host genes Downregulated host genes
Note 学位審査副論文
Published Date 2012-07
Publication Title Virus Research
Volume volume167
Issue issue1
Publisher Elsevier Science
Start Page 74
End Page 85
ISSN 0168-1702
NCID AA10642076
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version author
PubMed ID 22579597
DOI 10.1016/j.virusres.2012.04.008
Web of Sience KeyUT 000305496700010
Related Url https://doi.org/10.1016/j.virusres.2012.04.008 http://ousar.lib.okayama-u.ac.jp/54271
Author Kato, Nobuyuki| Sejima, Hiroe| Ueda, Youki| Mori, Kyoko| Satoh, Shinya| Dansako, Hiromichi| Ikeda, Masanori|
Published Date 2014-03-13
Publication Title PLOS ONE
Volume volume9
Issue issue3
Content Type Journal Article
Author Ueda, Youki| Takeda, Midori| Mori, Kyoko| Dansako, Hiromichi| Wakita, Takaji| Kim, Hye-Sook| Sato, Akira| Wataya, Yusuke| Ikeda, Masanori| Kato, Nobuyuki|
Published Date 2013-08-30
Publication Title PLOS ONE
Volume volume8
Issue issue8
Content Type Journal Article
Author Dansako, Hiromichi| Ueda, Youki| Okumura, Nobuaki| Satoh, Shinya| Sugiyama, Masaya| Mizokami, Masashi| Ikeda, Masanori| Kato, Nobuyuki|
Published Date 2015
Publication Title The FEBS journal
Content Type Journal Article
JaLCDOI 10.18926/AMO/53335
FullText URL 69_2_71.pdf
Author Hiramoto, Hiroki| Dansako, Hiromichi| Takeda, Midori| Satoh, Shinya| Wakita, Takaji| Ikeda, Masanori| Kato, Nobuyuki|
Abstract Persistent infection with hepatitis C virus (HCV) often causes chronic hepatitis, and then shows a high rate of progression to liver cirrhosis and hepatocellular carcinoma. To clarify the mechanism of the persistent HCV infection is considered to be important for the discovery of new target(s) for the development of anti-HCV strategies. In the present study, we found that the expression level of annexin A1 (ANXA1) in human hepatoma cell line Li23-derived D7 cells was remarkably lower than that in parental Li23 cells, whereas the susceptibility of D7 cells to HCV infection was much higher than that of Li23 cells. Therefore, we hypothesized that ANXA1 negatively regulates persistent HCV infection through the inhibition of viral RNA replication. The results revealed that HCV production was significantly inhibited without a concomitant reduction in the amount of lipid droplets in the D7 cells stably expressing exogenous ANXA1. Further, we demonstrated that ANXA1 negatively regulated the step of viral RNA replication rather than that of viral entry in human hepatocytes. These results suggest that ANXA1 would be a novel target for the development of anti-HCV strategies.
Keywords HCV annexin A1 Li23 cell line Li23-derived D7 cells HCV-JFH-1
Amo Type Original Article
Published Date 2015-04
Publication Title Acta Medica Okayama
Volume volume69
Issue issue2
Publisher Okayama University Medical School
Start Page 71
End Page 78
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 25899628
Web of Sience KeyUT 000353181700001
Author Kuroki, Misao| Ariumi, Yasuo| Hijikata, Makoto| Ikeda, Masanori| Dansako, Hiromichi| Wakita, Takaji| Shimotohno, Kunitada| Kato, Nobuyuki|
Published Date 2013-01-11
Publication Title Biochemical and Biophysical Research Communications
Volume volume430
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/49042
FullText URL 66_6_461.pdf
Author Koike, Kazuko| Takaki, Akinobu| Kato, Nobuyuki| Ouchida, Mamoru| Kanzaki, Hirotaka| Yasunaka, Tetsuya| Shiraha, Hidenori| Miyake, Yasuhiro| Yamamoto, Kazuhide|
Abstract Hepatitis C virus (HCV) infection induces several changes in hepatocytes, such as oxidative stress, steatosis, and hepatocarcinogenesis. Although considerable progress has been made during recent years, the mechanisms underlying these functions remain unclear. We employed proteomic techniques in HCV replicon-harboring cells to determine the effects of HCV replication on host-cell protein expression. We examined two-dimensional electrophoresis (2-DE) and mass spectrometry to compare and identify differentially expressed proteins between HCV subgenomic replicon-harboring cells and their “cured” cells. One of the identified proteins was confirmed using enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Full-length HCV genome RNA replicating and cured cells were also assessed using ELISA. Replicon-harboring cells showed higher expression of retinal dehydrogenase 1 (RALDH-1), which converts retinol to retinoic acid, and the cured cells showed higher expression of retinol-binding protein (RBP), which transports retinol from the liver to target tissues. The alteration in RBP expression was also confirmed by ELISA and Western blot analysis. We conclude that protein expression profiling demonstrated that HCV replicon eradication affected retinol-related protein expression.
Keywords hepatitis C virus retinol-binding protein
Amo Type Original Article
Published Date 2012-12
Publication Title Acta Medica Okayama
Volume volume66
Issue issue6
Publisher Okayama University Medical School
Start Page 461
End Page 468
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23254580
Web of Sience KeyUT 000312966100005
Author Ueda, Youki| Mori, Kyoko| Ariumi, Yasuo| Ikeda, Masanori| Kato, Nobuyuki|
Published Date 2011-06-17
Publication Title Biochemical and Biophysical Research Communications
Volume volume409
Issue issue4
Content Type Journal Article
JaLCDOI 10.18926/AMO/32281
FullText URL fulltext.pdf
Author Nozaki, Akito| Naganuma, Atsushi| Nakamura, Takashi| Tanaka, Katsuaki| Sekihara, Hisahiko| Kato, Nobuyuki|
Abstract <p>We have developed a reliable internally controlled RT-nested PCR method for the detection of hepatitis C virus (HCV) RNA using in vitro synthesized Renilla luciferase (Rluc) RNA as an internal control. Using this method, the 5'-noncoding region of HCV RNA (144 nucleotides) and Rluc RNA (276 nucleotides) were efficiently amplified in a single tube, and the sensitivity and specificity of this method were comparable to standard RT-nested PCR. This method was successfully performed on RNA specimens obtained from in vitro HCV-infected human hepatocyte PH5CH8 cells, which support HCV replication. In addition, we demonstrated that this method was useful for the evaluation of antiviral reagents by confirming the anti-HCV activity of bovine lactoferrin, which we previously found to be a new inhibitor of HCV infection. Therefore, this method may be useful for the studies of not only HCV but also of other viruses.</p>
Keywords Hepatitis C virus Reverse transcriptionnested PCR (RT-nested PCR) internal control
Amo Type Article
Published Date 2000-12
Publication Title Acta Medica Okayama
Volume volume54
Issue issue6
Publisher Okayama University Medical School
Start Page 253
End Page 257
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 11132918
Web of Sience KeyUT 000166042900003
JaLCDOI 10.18926/AMO/32025
FullText URL fulltext.pdf
Author Kato, Nobuyuki|
Abstract <p>Hepatitis C virus (HCV), discovered in 1989, is the major causative agent of parenteral non-A, non-B hepatitis worldwide. Following the development of a method of diagnosing HCV infection, it became apparent that HCV frequently causes chronic hepatitis. Persistent infection with HCV is implicated in liver cirrhosis and hepatocellular carcinoma. Current worldwide estimations suggest that more than 170 million people have been infected with HCV, an enveloped positive single-stranded RNA (9.6-kilobases) virus belonging to the Flaviviridae. The HCV genome shows remarkable sequence variation, especially in the hypervariable region 1 of the E2 protein-encoding region, and globally, HCV appears to be distributed with more than 30 genotypes. Complicated &#34;quasispecies&#34; and frequent mutations of viral genomes have also emerged. The HCV genome encodes a large polyprotein precursor of about 3,000 amino acid residues, and this precursor protein is cleaved by the host and viral proteinases to generate at least 10 proteins in the following order: NH2-core-envelope (E1)-E2-p7-nonstructural protein 2 (NS2)-NS3-NS4A-NS4B-NS5A-NS5B-COOH. These viral proteins not only function in viral replication but also affect a variety of cellular functions. Although several explanations have been proposed, the mechanisms of HCV infection and replication in targeted cells, the mechanism of persistent viral infection, and the pathogenesis of hepatic diseases (hepatitis or hepatocellular carcinoma) are all poorly understood. A major reason why these mechanisms remain unclear is the lack of a good experimental HCV replication system. Although several classical trials using cultured cells have been reported, several new, more promising experimental strategies (generations of infectious cDNA clone, replicon, animal models, etc.) are currently being designed and tested, in order to resolve these problems. In addition, new therapies for chronic hepatitis have also been developed. The enormous body of information collected thus far in the field of HCV research is summarized below, and an overview of the current status of HCV molecular virology of HCV is provided.&#60;/P&#62;</p>
Amo Type Review
Published Date 2001-06
Publication Title Acta Medica Okayama
Volume volume55
Issue issue3
Publisher Okayama University Medical School
Start Page 133
End Page 159
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 11434427
Web of Sience KeyUT 000169512600001
JaLCDOI 10.18926/AMO/31716
FullText URL fulltext.pdf
Author Alam, Shahjalal S.| Nakamura, Takashi| Naganuma, Atsushi| Nozaki, Akito| Nouso, Kazuhiro| Shimomura, Hiroyuki| Kato, Nobuyuki|
Abstract <p>We have shown that highly proofreading DNA polymerase is required for the polymerase chain reaction in the genetic analysis of hepatitis C virus (HCV). To clarify the status of HCV quasispecies in hepatic tissue using proofreading DNA polymerase, we performed a genetic analysis of the HCV core protein-encoding region in cancerous and noncancerous lesions derived from 4 patients with hepatocellular carcinoma. In contrast to the previously published data, we observed neither deletions nor stop codons in the analyzed region and no significant difference in the complexity of HCV quasispecies between cancerous and noncancerous lesions. This result suggests that the HCV core gene is never structurally defective in hepatic tissues, including cancerous lesions. However, in 3 of the patients, the consensus HCV species differed between cancerous and noncancerous lesions, suggesting that the predominant replicating HCV species differs between these 2 types of lesions. Moreover, during the course of the study, we obtained several interesting variants possessing a substitution at codon 9 of the core gene, whose substitution has been shown to induce the production of the F protein synthesized by a - 2/+1 ribosomal frameshift.</p>
Keywords hepatitis C virus core gene hepatocellular carcinoma quasispecies proofreading DNA polymerase
Amo Type Article
Published Date 2002-06
Publication Title Acta Medica Okayama
Volume volume56
Issue issue3
Publisher Okayama University Medical School
Start Page 141
End Page 147
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12108585
Web of Sience KeyUT 000176521200004
JaLCDOI 10.18926/AMO/31696
FullText URL fulltext.pdf
Author Nozaki, Akito| Kato, Nobuyuki|
Abstract <p>Based on recent LightCycler techniques developed for the quantitation of serum HCV RNA, we have developed a quantitative method for the intracellular hepatitis C virus (HCV) RNA using LightCycler PCR. A simple real-time PCR assay, based on the SYBR Green I dye and LightCycler fluorimeter and with no probe requirement, is described. In the presence of 0.5 microg of cellular RNA, it was demonstrated that as few as 25 copies of HCV RNA could be specifically detected with a set of primers that amplify a 144-base pair sequence unique to the 5'-noncoding region of HCV RNA. We demonstrated that this method was useful for the evaluation of antiviral reagents using HCV-infected human cultured cells.</p>
Keywords hepatitis C virus real-time PCR LightCycler
Amo Type Article
Published Date 2002-04
Publication Title Acta Medica Okayama
Volume volume56
Issue issue2
Publisher Okayama University Medical School
Start Page 107
End Page 110
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12002616
Web of Sience KeyUT 000175176900007
Author Ariumi, Yasuo| Kuroki, Misao| Dansako, Hiromichi| Abe, Kenichi| Ikeda, Masanori| Wakita, Takaji| Kato, Nobuyuki|
Published Date 2010-04-01
Publication Title 岡山医学会雑誌
Volume volume122
Issue issue1
Content Type Journal Article
Author 加藤 宣之| 小熊 惠二|
Published Date 2001-04-28
Publication Title 岡山医学会雑誌
Volume volume113
Issue issue1
Content Type Journal Article