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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
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Rapamycin enhances HBV production by inducing cellular autophagy
Wenjuan Huang1, Fengrong Zhao2, Ying Huang3
1Department of Laboratory Medicine, Affiliated to the Second Hospital Chongqing Medical University, Chongqing, China.
Hepatitis Monthly
|November 25, 2014
Summary
Rapamycin reactivates Hepatitis B virus (HBV) infection by inducing cellular autophagy. Autophagy inhibition reversed this effect, suggesting a mechanism for HBV reactivation in patients receiving rapamycin.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Reports suggest rapamycin may reactivate Hepatitis B virus (HBV) infection.
- The underlying mechanism for this reactivation remains unclear.
Purpose of the Study:
- To investigate how rapamycin enhances HBV replication and expression.
- To elucidate the role of cellular autophagy in rapamycin-induced HBV reactivation.
Main Methods:
- HepG2.2.15 cells were treated with rapamycin to induce autophagy.
- Autophagy was assessed via microscopy and Western blotting for LC3-II/LC3-I.
- HBV DNA, mRNA, and HBsAg levels were quantified using PCR, Southern blotting, and ELISA.
Main Results:
- Rapamycin treatment increased HBV DNA and HBsAg levels in HepG2.2.15 cells.
- The autophagy inhibitor 3-methyladenine (3-MA) reversed these increases.
- These findings link rapamycin-induced autophagy to enhanced HBV replication.
Conclusions:
- Cellular autophagy induced by rapamycin contributes to HBV replication and expression.
- This study provides a potential explanation for HBV reactivation in patients undergoing rapamycin therapy.
- Targeting autophagy may offer a strategy to manage HBV reactivation.
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