HCV Induces Stress and Cell Death in Infected Mice
Author Information
Author(s): Joyce Michael A., Walters Kathie-Anne, Lamb Sue-Ellen, Yeh Mathew M., Zhu Lin-Fu, Kneteman Norman, Doyle Jason S., Katze Michael G., Tyrrell D. Lorne
Primary Institution: University of Alberta
Hypothesis
HCV infection leads to hepatocyte damage and apoptosis through the induction of oxidative and endoplasmic reticulum stress.
Conclusion
HCV infection contributes to liver cell damage and apoptosis by inducing stress while inhibiting protective anti-apoptotic mechanisms.
Supporting Evidence
- HCV infection led to increased apoptosis in liver cells.
- Oxidative stress and ER stress were identified as key factors in cell death.
- Gene expression profiling showed activation of innate antiviral signaling pathways.
- Increased levels of pro-apoptotic BAX were observed in infected cells.
- Anti-apoptotic factors like NF-κB and BCL-xL were decreased in HCV-infected cells.
- Histological analysis revealed signs of hepatocyte damage and inflammation.
- FAS expression was elevated in infected cells, correlating with apoptosis.
- Chimeric mice model effectively mimicked human HCV infection responses.
Takeaway
Hepatitis C virus can make liver cells sick and die by causing stress inside the cells, even without the immune system being involved.
Methodology
The study used chimeric SCID/Alb-uPA mice infected with HCV to analyze gene expression and apoptosis in liver cells.
Potential Biases
Potential bias in interpreting results due to the use of a specific mouse model that may not capture all human disease complexities.
Limitations
The study is limited to a mouse model and may not fully represent human responses to HCV infection.
Participant Demographics
Chimeric SCID/Alb-uPA mice with human hepatocytes.
Statistical Information
P-Value
≤0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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