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Volume 14
Issue 11
10.3390/v14112521
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Article

Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo

by
Savvina Moustafa
1,
Katerina Kassela
1,2,
Maria Bampali
2,
Nikolas Dovrolis
2,
Athanassios Kakkanas
1,
Apostolos Beloukas
3,4,
Penelope Mavromara
1,5 and
Ioannis Karakasiliotis
1,2,*
1
Molecular Virology Laboratory, Department of Microbiology, Hellenic Pasteur Institute, 11521 Athens, Greece
2
Laboratory of Biology, Department of Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece
3
National AIDS Reference Center of Southern Greece, Department of Public Health Policy, University of West Attica, 12243 Athens, Greece
4
Molecular Microbiology & Immunology Lab, Department of Biomedical Sciences, University of West Attica, 11521 Athens, Greece
5
Department of Molecular Biology and Genetics, Democritus University of Thrace, 68100 Alexandroupolis, Greece
*
Author to whom correspondence should be addressed.
Viruses 2022, 14(11), 2521; https://doi.org/10.3390/v14112521
Submission received: 21 August 2022 / Revised: 1 November 2022 / Accepted: 10 November 2022 / Published: 14 November 2022
(This article belongs to the Special Issue State-of-the-Art Virus Research in Greece)
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Abstract

Hepatitis C virus (HCV) core protein is a multifunctional protein that is involved in the proliferation, inflammation, and apoptosis mechanism of hepatocytes. HCV core protein genetic variability has been implicated in various outcomes of HCV pathology and treatment. In the present study, we aimed to analyze the role of the HCV core protein in tumor necrosis factor α (TNFα)-induced death under the viewpoint of HCV genetic variability. Immortalized hepatocytes (IHH), and not the Huh 7.5 hepatoma cell line, stably expressing HCV subtype 4a and HCV subtype 4f core proteins showed that only the HCV 4a core protein could increase sensitivity to TNFα-induced death. Development of two transgenic mice expressing the two different core proteins under the liver-specific promoter of transthyretin (TTR) allowed for the in vivo assessment of the role of the core in TNFα-induced death. Using the TNFα-dependent model of lipopolysaccharide/D-galactosamine (LPS/Dgal), we were able to recapitulate the in vitro results in IHH cells in vivo. Transgenic mice expressing the HCV 4a core protein were more susceptible to the LPS/Dgal model, while mice expressing the HCV 4f core protein had the same susceptibility as their littermate controls. Transcriptome analysis in liver biopsies from these transgenic mice gave insights into HCV core molecular pathogenesis while linking HCV core protein genetic variability to differential pathology in vivo.
Keywords: hepatitis C virus; core protein; TNFα hepatitis C virus; core protein; TNFα

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MDPI and ACS Style

Moustafa, S.; Kassela, K.; Bampali, M.; Dovrolis, N.; Kakkanas, A.; Beloukas, A.; Mavromara, P.; Karakasiliotis, I. Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo. Viruses 2022, 14, 2521. https://doi.org/10.3390/v14112521

AMA Style

Moustafa S, Kassela K, Bampali M, Dovrolis N, Kakkanas A, Beloukas A, Mavromara P, Karakasiliotis I. Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo. Viruses. 2022; 14(11):2521. https://doi.org/10.3390/v14112521

Chicago/Turabian Style

Moustafa, Savvina, Katerina Kassela, Maria Bampali, Nikolas Dovrolis, Athanassios Kakkanas, Apostolos Beloukas, Penelope Mavromara, and Ioannis Karakasiliotis. 2022. "Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo" Viruses 14, no. 11: 2521. https://doi.org/10.3390/v14112521

APA Style

Moustafa, S., Kassela, K., Bampali, M., Dovrolis, N., Kakkanas, A., Beloukas, A., Mavromara, P., & Karakasiliotis, I. (2022). Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo. Viruses, 14(11), 2521. https://doi.org/10.3390/v14112521

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