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  1. Book: Human oncogenic viruses

    Ou, Jing-Hsiung James

    2010  

    Author's details eds. Jing-Hsiung James Ou
    Keywords Oncogenic viruses
    Subject code 616.994019
    Language English
    Size XIV, 339 S. : Ill., graph. Darst.
    Publisher World Scientific
    Publishing place New Jersey u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT016005503
    ISBN 978-981-283-346-4 ; 981-283-346-3
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Regulation of Mitochondrial Metabolism by Hepatitis B Virus.

    Li, Yumei / Ou, Jing-Hsiung James

    Viruses

    2023  Volume 15, Issue 12

    Abstract: Mitochondria play important roles in the synthesis of ATP, the production of reactive oxygen species, and the regulation of innate immune response and apoptosis. Many viruses perturb mitochondrial activities to promote their replication and cause cell ... ...

    Abstract Mitochondria play important roles in the synthesis of ATP, the production of reactive oxygen species, and the regulation of innate immune response and apoptosis. Many viruses perturb mitochondrial activities to promote their replication and cause cell damage. Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases, including cirrhosis and hepatocellular carcinoma (HCC). This virus can also alter mitochondrial functions and metabolism to promote its replication and persistence. In this report, we summarize recent research progress on the interaction between HBV and mitochondrial metabolism, as well as the effect this interaction has on HBV replication and persistence.
    MeSH term(s) Humans ; Hepatitis B virus/physiology ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Liver Cirrhosis/complications ; Reactive Oxygen Species ; Hepatitis B ; Hepatitis B, Chronic
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2023-11-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v15122359
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Regulators of liver cancer stem cells.

    Liu, Kai / Ou, Jing-Hsiung James

    World journal of stem cells

    2021  Volume 13, Issue 8, Page(s) 1127–1133

    Abstract: Hepatocellular carcinoma (HCC) is a leading cause of cancer deaths. It is often detected at a stage when there are few therapeutic options. Liver cancer stem cells (LCSCs) are highly tumorigenic and resistant to chemotherapy and radiation therapy. Their ... ...

    Abstract Hepatocellular carcinoma (HCC) is a leading cause of cancer deaths. It is often detected at a stage when there are few therapeutic options. Liver cancer stem cells (LCSCs) are highly tumorigenic and resistant to chemotherapy and radiation therapy. Their presence in HCC is a major reason why HCC is difficult to treat. The development of LCSCs is regulated by a variety of factors. This review summarizes recent advances on the factors that regulate the development of LCSCs. Due to the importance of LCSCs in the development of HCC, a better understanding of how LCSCs are regulated will help to improve the treatments for HCC patients.
    Language English
    Publishing date 2021-09-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2583482-4
    ISSN 1948-0210
    ISSN 1948-0210
    DOI 10.4252/wjsc.v13.i8.1127
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Pathogenicity and virulence of Hepatitis B virus.

    Chuang, Yu-Chen / Tsai, Kuen-Nan / Ou, Jing-Hsiung James

    Virulence

    2022  Volume 13, Issue 1, Page(s) 258–296

    Abstract: Hepatitis B virus (HBV) is a hepatotropic virus and an important human pathogen. There are an estimated 296 million people in the world that are chronically infected by this virus, and many of them will develop severe liver diseases including hepatitis, ... ...

    Abstract Hepatitis B virus (HBV) is a hepatotropic virus and an important human pathogen. There are an estimated 296 million people in the world that are chronically infected by this virus, and many of them will develop severe liver diseases including hepatitis, cirrhosis and hepatocellular carcinoma (HCC). HBV is a small DNA virus that replicates via the reverse transcription pathway. In this review, we summarize the molecular pathways that govern the replication of HBV and its interactions with host cells. We also discuss viral and non-viral factors that are associated with HBV-induced carcinogenesis and pathogenesis, as well as the role of host immune responses in HBV persistence and liver pathogenesis.
    MeSH term(s) Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Hepatitis B virus/genetics ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Virulence
    Language English
    Publishing date 2022-05-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2657572-3
    ISSN 2150-5608 ; 2150-5594
    ISSN (online) 2150-5608
    ISSN 2150-5594
    DOI 10.1080/21505594.2022.2028483
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Autophagy in HCV Replication and Protein Trafficking.

    Chu, Ja Yeon Kim / Ou, Jing-Hsiung James

    International journal of molecular sciences

    2021  Volume 22, Issue 3

    Abstract: Autophagy is a catabolic process that is important for maintaining cellular homeostasis. It is also known to possess other functions including protein trafficking and anti-microbial activities. Hepatitis C virus (HCV) is known to co-opt cellular ... ...

    Abstract Autophagy is a catabolic process that is important for maintaining cellular homeostasis. It is also known to possess other functions including protein trafficking and anti-microbial activities. Hepatitis C virus (HCV) is known to co-opt cellular autophagy pathway to promote its own replication. HCV regulates autophagy through multiple mechanisms to control intracellular protein and membrane trafficking to enhance its replication and suppress host innate immune response. In this review, we discuss the current knowledge on the interplay between HCV and autophagy and the crosstalk between HCV-induced autophagy and host innate immune responses.
    MeSH term(s) Autophagy/physiology ; Cell Membrane/metabolism ; Hepacivirus/physiology ; Hepatitis C/pathology ; Hepatitis C/virology ; Hepatocytes/virology ; Homeostasis ; Humans ; Immunity, Innate ; Membrane Microdomains ; Mitochondria/metabolism ; Mitophagy ; Protein Transport ; RNA, Viral/metabolism ; Signal Transduction ; Virus Replication
    Chemical Substances RNA, Viral
    Language English
    Publishing date 2021-01-22
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22031089
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Biographical Feature: James H. Strauss, Jr. (1938-2021).

    Ou, Jing-Hsiung James / Kuhn, Richard J / Lopez, Susana / Rice, Charles M

    Journal of virology

    2022  Volume 96, Issue 9, Page(s) e0015522

    Language English
    Publishing date 2022-04-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.00155-22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Hepatitis B virus e antigen and viral persistence.

    Tsai, Kuen-Nan / Ou, Jing-Hsiung James

    Current opinion in virology

    2021  Volume 51, Page(s) 158–163

    Abstract: Hepatitis B virus (HBV) e antigen (HBeAg) was discovered in the sera of HBV patients nearly 50 years ago. It is not essential for HBV to infect or replicate in hepatocytes. Earlier clinical studies suggested that this antigen might play an important role ...

    Abstract Hepatitis B virus (HBV) e antigen (HBeAg) was discovered in the sera of HBV patients nearly 50 years ago. It is not essential for HBV to infect or replicate in hepatocytes. Earlier clinical studies suggested that this antigen might play an important role for HBV to establish persistence in babies after its mother-to-child transmission. Subsequent clinical studies also suggested that HBeAg might have immunomodulatory activities. In recent years, a large body of information on how HBeAg might modulate host immunity was published. In this review, we summarize recent research progresses on the immunomodulatory activities of HBeAg and discuss how these activities of HBeAg may promote HBV persistence.
    MeSH term(s) Hepatitis B e Antigens/immunology ; Hepatitis B virus/immunology ; Hepatitis B virus/pathogenicity ; Hepatitis B, Chronic/immunology ; Hepatitis B, Chronic/virology ; Humans ; Immunomodulation ; Infectious Disease Transmission, Vertical
    Chemical Substances Hepatitis B e Antigens
    Language English
    Publishing date 2021-10-28
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2611378-8
    ISSN 1879-6265 ; 1879-6257
    ISSN (online) 1879-6265
    ISSN 1879-6257
    DOI 10.1016/j.coviro.2021.10.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Regulation of Autophagy by Hepatitis C Virus for Its Replication.

    Wang, Linya / Ou, Jing-Hsiung James

    DNA and cell biology

    2018  Volume 37, Issue 4, Page(s) 287–290

    Abstract: Macroautophagy, hereafter autophagy, is a catabolic process that is important for maintaining cellular homeostasis. It can also be used by cells to remove intracellular microbial pathogens. However, the studies on hepatitis C virus (HCV) in recent years ... ...

    Abstract Macroautophagy, hereafter autophagy, is a catabolic process that is important for maintaining cellular homeostasis. It can also be used by cells to remove intracellular microbial pathogens. However, the studies on hepatitis C virus (HCV) in recent years indicated that this virus could regulate this cellular pathway and use it to enhance its replication. HCV could temporally control the autophagic flux and use the autophagic membranes for the assembly of its RNA replication complex. In this report, we will discuss the biogenesis of autophagosomes induced by HCV and how HCV uses this autophagic pathway for its RNA replication.
    MeSH term(s) Autophagosomes ; Autophagy/immunology ; Autophagy/physiology ; DNA Replication ; Hepacivirus/metabolism ; Hepacivirus/pathogenicity ; Humans ; Phagosomes/metabolism ; RNA, Viral/genetics ; RNA, Viral/metabolism ; RNA, Viral/physiology ; Virus Replication/genetics ; Virus Replication/physiology
    Chemical Substances RNA, Viral
    Language English
    Publishing date 2018-01-19
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1024454-2
    ISSN 1557-7430 ; 0198-0238 ; 1044-5498
    ISSN (online) 1557-7430
    ISSN 0198-0238 ; 1044-5498
    DOI 10.1089/dna.2017.4115
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Mechanisms of Hepatitis B Virus-Induced Hepatocarcinogenesis.

    Lee, Jiyoung / Tsai, Kuen-Nan / Ou, Jing-Hsiung James

    Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer

    2020  Volume 217, Page(s) 47–70

    Abstract: Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). There are approximately 250 million people in the world that are chronically infected by this virus, resulting in nearly 1 million deaths every year. Many of these patients die ... ...

    Abstract Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). There are approximately 250 million people in the world that are chronically infected by this virus, resulting in nearly 1 million deaths every year. Many of these patients die from severe liver diseases, including HCC. HBV may induce HCC through the induction of chronic liver inflammation, which can cause oxidative stress and DNA damage. However, many studies also indicated that HBV could induce HCC via the alteration of hepatocellular physiology that may involve genetic and epigenetic changes of the host DNA, the alteration of cellular signaling pathways, and the inhibition of DNA repair mechanisms. This alteration of cellular physiology can lead to the accumulation of DNA damages and the promotion of cell cycles and predispose hepatocytes to oncogenic transformation.
    MeSH term(s) Carcinoma, Hepatocellular/virology ; DNA Repair ; Hepatitis B/complications ; Hepatitis B/genetics ; Hepatitis B virus/genetics ; Hepatitis B virus/pathogenicity ; Humans ; Liver Neoplasms/virology ; Oncogenes
    Language English
    Publishing date 2020-11-13
    Publishing country Germany
    Document type Journal Article
    ISSN 0080-0015
    ISSN 0080-0015
    DOI 10.1007/978-3-030-57362-1_3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Analysis of the interplay between hepatitis B virus-positive hepatocytes and Kupffer cells

    Li, Yumei / Lee, Jiyoung / Helou, Doumet Georges / Akbari, Omid / Ou, Jing-Hsiung James

    STAR protocols

    2022  Volume 3, Issue 2, Page(s) 101364

    Abstract: Kupffer cells play critical roles in both hepatitis B virus (HBV) persistence and clearance. Here, we provide a protocol for studying the interplay between Kupffer cells and HBV-positive ... ...

    Abstract Kupffer cells play critical roles in both hepatitis B virus (HBV) persistence and clearance. Here, we provide a protocol for studying the interplay between Kupffer cells and HBV-positive hepatocytes
    MeSH term(s) Animals ; Hepatitis B virus/genetics ; Hepatocytes ; Kupffer Cells ; Liver ; Mice ; Perfusion
    Language English
    Publishing date 2022-05-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2022.101364
    Database MEDical Literature Analysis and Retrieval System OnLINE

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