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Hepatitis C viral proteins affect cell viability and membrane permeability.
G Kalkeri1, N Khalap, S Akhter
1Department of Pathology and Laboratory Medicine, Tulane University Health Science Center, New Orleans, Louisiana 70112, USA.
Experimental and Molecular Pathology
|December 6, 2001
Summary
Hepatitis C virus (HCV) proteins induce cell death in liver cells. This study shows that expressing all HCV proteins triggers apoptosis, a key factor in chronic hepatitis C infection.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis C virus (HCV) infection is a major cause of chronic liver disease.
- The specific mechanisms by which HCV proteins impact host cell viability are not fully understood.
Purpose of the Study:
- To investigate the effects of expressing all structural and nonstructural hepatitis C virus proteins on the viability of hepatic cells.
- To elucidate the role of HCV protein expression in inducing cell death pathways.
Main Methods:
- Huh-7 cells were transfected with a full-length HCV cDNA clone for protein expression.
- HCV protein expression was facilitated by a replication-defective adenovirus encoding T7 RNA polymerase.
- Cell viability was assessed using trypan blue assay, flow cytometry, cell cycle analysis, TUNEL assay, and microscopy.
Main Results:
- Expression of full-length HCV proteins significantly reduced cell viability.
- Cells expressing HCV proteins exhibited loss of membrane permeability and apoptotic cell death.
- Apoptosis was confirmed by sub-G0 cell cycle peak, DNA fragmentation, and nuclear condensation.
Conclusions:
- Expression of all structural and nonstructural HCV proteins in hepatic cells induces apoptotic cell death.
- This induction of apoptosis is a significant event potentially contributing to the pathogenesis of chronic hepatitis C infection in humans.