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The Multiple Roles of Hepatitis B Virus X Protein (HBx) Dysregulated MicroRNA in Hepatitis B Virus-Associated Hepatocellular Carcinoma (HBV-HCC) and Immune Pathways

  1. Author:
    Sartorius, Kurt
    Swadling, Leo
    An,Ping
    Makarova, Julia
    Winkler,Cheryl
    Chuturgoon, Anil
    Kramvis, Anna
  2. Author Address

    Univ Witwatersrand, Fac Commerce Law & Management, ZA-2050 Johannesburg, South Africa.Univ KwaZulu Natal, Sch Nursing & Publ Hlth, Dept Publ Hlth Med, ZA-4041 Durban, South Africa.UKZN Gastrointestinal Canc Res Ctr, ZA-4041 Durban, South Africa.UCL, Div Infect & Immun, Mortimer St, London WC1E 6BT, England.Leidos Biomed Res Inc, NCI, Basic Res Lab, Frederick Nat Lab Canc Res,Ctr Canc Res, Frederick, MD 20878 USA.Natl Res Univ Higher Sch Econ, Fac Biol & Biotechnol, Moscow 10100, Russia.Univ Witwatersrand, Hepatitis Virus Divers Res Unit, Dept Internal Med, Sch Clin Med,Fac Hlth Sci, ZA-2050 Johannesburg, South Africa.
    1. Year: 2020
    2. Date: JUL
    3. Epub Date: 2020 07 10
  1. Journal: Viruses
  2. MDPI,
    1. 12
    2. 7
  3. Type of Article: Review
  4. Article Number: ARTN 746
  5. ISSN: 1999-4915
  1. Abstract:

    Currently, the treatment of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) [HBV-HCC] relies on blunt tools that are unable to offer effective therapy for later stage pathogenesis. The potential of miRNA to treat HBV-HCC offer a more targeted approach to managing this lethal carcinoma; however, the complexity of miRNA as an ancillary regulator of the immune system remains poorly understood. This review examines the overlapping roles of HBx-dysregulated miRNA in HBV-HCC and immune pathways and seeks to demonstrate that specific miRNA response in immune cells is not independent of their expression in hepatocytes. This interplay between the two pathways may provide us with the possibility of using candidate miRNA to manipulate this interaction as a potential therapeutic option.

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External Sources

  1. DOI: 10.3390/v12070746
  2. PMID: 32664401
  3. WOS: 000556521300001

Library Notes

  1. Fiscal Year: FY2019-2020
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