Axin expression delays herpes simplex virus-induced autophagy and enhances viral replication in L929 cells
- Authors
- Choi, Eun-Jin; Kee, Sun-Ho
- Issue Date
- 2월-2014
- Publisher
- WILEY-BLACKWELL
- Keywords
- autophagy; axin; herpes simplex virus
- Citation
- MICROBIOLOGY AND IMMUNOLOGY, v.58, no.2, pp.103 - 111
- Indexed
- SCIE
SCOPUS
- Journal Title
- MICROBIOLOGY AND IMMUNOLOGY
- Volume
- 58
- Number
- 2
- Start Page
- 103
- End Page
- 111
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/99475
- DOI
- 10.1111/1348-0421.12123
- ISSN
- 0385-5600
- 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.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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