@article{mbs:/content/journal/jgv/10.1099/vir.0.051540-0, author = "Choi, Eun-Jin and Kim, Sewoon and Jho, Eek-hoon and Song, Ki-Joon and Kee, Sun-Ho", title = "Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells", journal= "Journal of General Virology", year = "2013", volume = "94", number = "7", pages = "1636-1646", doi = "https://doi.org/10.1099/vir.0.051540-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.051540-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", 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.", }