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Published on: August 30, 2017
Axin expression delays herpes simplex virus-induced autophagy and enhances viral replication in L929 cells
1Laboratory of Cell Biology, Department of Microbiology and Bank for Pathogenic Virus, College of Medicine, Korea University, Seoul, 136-705, Korea.
Abstract:
Axin, a negative regulator of the Wnt signaling pathway, plays a critical role in various cellular events including cell proliferation and cell death. Axin-regulated cell death affects multiple processes, including viral replication. For example, axin expression suppresses herpes simplex virus (HSV)-induced necrotic cell death and enhances viral replication. Based on these observations, this study investigated the involvement of autophagy in regulation of HSV replication and found axin expression inhibits autophagy-mediated suppression of viral replication in L929 cells. HSV infection induced autophagy in a time- and viral dose-dependent manner in control L929 cells (L-EV), whereas virus-induced autophagy was delayed in axin-expressing L929 cells (L-axin). Subsequent analysis showed that induction of autophagy by rapamycin reduced HSV replication, and that inhibiting autophagy by 3-methyladenine (3MA) and beclin-1 knockdown facilitated viral replication in L-EV cells. In addition, preventing autophagy with 3MA suppressed virus-induced cytotoxicity in L-EV cells. In contrast, HSV replication in L-axin cells was resistant to changes in autophagy. These results suggest that axin expression may render L929 cells resistant to HSV-infection induced autophagy, leading to enhanced viral replication.
Insights
Axin protein expression suppresses autophagy, a cellular process that normally limits viral replication. This leads to increased herpes simplex virus (HSV) replication in cells expressing axin.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Axin is a key negative regulator of the Wnt signaling pathway.
- Axin influences cellular events like proliferation and cell death, impacting viral replication.
- Axin expression has been shown to suppress herpes simplex virus (HSV)-induced cell death and enhance viral replication.
Purpose of the Study:
- To investigate the role of autophagy in regulating HSV replication.
- To determine how axin expression affects autophagy-induced suppression of HSV replication.
Main Methods:
- Utilized L929 cell lines with and without axin expression (L-EV and L-axin).
- Assessed HSV-induced autophagy in response to viral infection and dose.
- Manipulated autophagy levels using rapamycin (induction) and 3-methyladenine (inhibition).
- Examined the effect of beclin-1 knockdown on viral replication.
Main Results:
- HSV infection induced autophagy in control L929 cells in a time- and dose-dependent manner.
- Axin expression in L929 cells delayed the induction of autophagy by HSV.
- Autophagy induction reduced HSV replication, while inhibition facilitated it in control cells.
- HSV replication in axin-expressing cells was unaffected by autophagy modulation.
- Inhibition of autophagy reduced HSV-induced cytotoxicity in control cells.
Conclusions:
- Axin expression inhibits autophagy-mediated suppression of HSV replication.
- Axin may confer resistance to HSV-induced autophagy in L929 cells, enhancing viral replication.
- Autophagy plays a significant role in controlling HSV replication and associated cytotoxicity.
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