ArticleScientific reports2017
Oxidative Stress and Immune Responses During Hepatitis C Virus Infection in Tupaia belangeri.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Natural Hepacivirus Infection in Tree Shrews: A Call for Routine Screening in Hepatitis Virus Research.Viruses · 2025Article
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Toll-like Receptor Response to Human Immunodeficiency Virus Type 1 or Co-Infection with Hepatitis B or C Virus: An Overview.International journal of molecular sciences · 2023Review
- TLR agonists as vaccine adjuvants in the prevention of viral infections: an overview.Frontiers in microbiology · 2023Review
- Epidemiology and Risk Factors for Acute Viral Hepatitis in Bangladesh: An Overview.Microorganisms · 2022Review
- Toll-like Receptor Response to Hepatitis C Virus Infection: A Recent Overview.International journal of molecular sciences · 2022Review
- Chinese Tea Alleviates CClNutrients · 2022Article
- Molecular cloning and characterization of NPC1L1 in the Chinese tree shrew (Tupaia belangeri chinensis).Molecular biology reports · 2021Article
- Tree Shrew as an Emerging Small Animal Model for Human Viral Infection: A Recent Overview.Viruses · 2021Review
- The Impact of Hepatitis C Virus Genotypes on Oxidative Stress Markers and Catalase Activity.Oxidative medicine and cellular longevity · 2021Article
- Mayaro Virus Pathogenesis and Transmission Mechanisms.Pathogens (Basel, Switzerland) · 2020Review
- Pathological and genetic aspects of spontaneous mammary gland tumor in Tupaia belangeri (tree shrew).PloS one · 2020Article
- Pathogenesis and Immune Response Caused by Vector-Borne and Other Viral Infections in aMicroorganisms · 2019Review
- Hepatitis C virus core or NS3/4A protein expression preconditions hepatocytes against oxidative stress and endoplasmic reticulum stress.Redox report : communications in free radical research · 2019Article
- Mayaro Virus Induction of Oxidative Stress is Associated With Liver Pathology in a Non-Lethal Mouse Model.Scientific reports · 2019Article
- Polyphenols in Liubao Tea Can Prevent CCl₄-Induced Hepatic Damage in Mice through Its Antioxidant Capacities.Nutrients · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is a leading cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma. To address the molecular basis of HCV pathogenesis using tupaias (Tupaia belangeri), we characterized host responses upon HCV infection. Adult tupaias were infected with HCV genotypes 1a, 1b, 2a, or 4a. Viral RNA, alanine aminotransferase, anti-HCV core and anti-nonstructural protein NS3 antibody titres, reactive oxygen species (ROS), and anti-3β-hydroxysterol-Δ24reductase (DHCR24) antibody levels were measured at 2-week intervals from 0 to 41 weeks postinfection. All HCV genotypes established infections and showed intermittent HCV propagation. Moreover, all tupaias produced anti-core and anti-NS3 antibodies. ROS levels in sera and livers were significantly increased, resulting in induction of DHCR24 antibody production. Similarly, lymphocytic infiltration, disturbance of hepatic cords, and initiation of fibrosis were observed in livers from HCV-infected tupaias. Intrahepatic levels of Toll-like receptors 3, 7, and 8 were significantly increased in all HCV-infected tupaias. However, interferon-β was only significantly upregulated in HCV1a- and HCV2a-infected tupaias, accompanied by downregulation of sodium taurocholate cotransporting polypeptide. Thus, our findings showed that humoral and innate immune responses to HCV infection, ROS induction, and subsequent increases in DHCR24 auto-antibody production occurred in our tupaia model, providing novel insights into understanding HCV pathogenesis.
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