HCV Causes Chronic Endoplasmic Reticulum Stress Leading to Adaptation
Author Information
Author(s): Merquiol Emmanuelle, Uzi Dotan, Mueller Tobias, Goldenberg Daniel, Nahmias Yaakov, Xavier Ramnik J., Tirosh Boaz, Shibolet Oren
Primary Institution: Hadassah-Hebrew University Medical Center, Jerusalem, Israel
Hypothesis
Does HCV induce chronic ER stress and adaptation mechanisms during infection?
Conclusion
HCV induces adaptation to chronic ER stress, which can be reversed upon viral suppression.
Supporting Evidence
- HCV infection activates UPR pathways including IRE1 and EIF2α.
- Chronic ER stress leads to reduced responsiveness to further drug-induced stress.
- Interferon treatment restores UPR responsiveness in HCV-infected cells.
Takeaway
HCV makes cells stressed for a long time, but they learn to cope with it. If the virus is stopped, the cells can respond better to stress again.
Methodology
The study used HuH7.5.1 cells and HCV-transgenic mice to analyze ER stress and UPR activation.
Limitations
The study primarily focused on specific cellular models and may not fully represent in vivo conditions.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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