Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells
- Authors
- Choi, Eun-Jin; Kim, Sewoon; Jho, Eek-hoon; Song, Ki-Joon; Kee, Sun-Ho
- Issue Date
- 7월-2013
- Publisher
- SOC GENERAL MICROBIOLOGY
- Citation
- JOURNAL OF GENERAL VIROLOGY, v.94, pp.1636 - 1646
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF GENERAL VIROLOGY
- Volume
- 94
- Start Page
- 1636
- End Page
- 1646
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/102869
- DOI
- 10.1099/vir.0.051540-0
- ISSN
- 0022-1317
- Abstract
- Herpes simplex virus type 1 (HSV-1) replicates in various cell types and induces early cell death, which limits viral replication in certain cell types. Axin is a scaffolding protein that regulates Wnt signalling and participates in various cellular events, including cellular proliferation and cell death. The effects of axin expression on HSV-1 infection were investigated based on our initial observation that Wnt3a treatment or axin knockdown reduced HSV-1 replication. L929 cells expressed the axin protein in a doxycycline-inducible manner (L-axin) and enhanced HSV-1 replication in comparison to control cells (L-EV). HSV-1 infection induced cell death as early as 6 h after infection through the necrotic pathway and required de novo protein synthesis in L929 cells. Subsequent analysis of viral protein expression suggested that axin expression led to suppression of HSV-1-induced premature cell death, resulting in increased late gene expression. In analysis of axin deletion mutants, the regulators of the G-protein signalling (RGS) domain were involved in the axin-mediated enhancement of viral replication and reduction in cell death. These results suggest that viral replication enhancement might be mediated by the axin RGS domain.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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