Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells

Eun Jin Choi, Sewoon Kim, Eek Hoon Jho, Ki-Joon Song, Sun-Ho Kee

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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.

Original languageEnglish
Pages (from-to)1636-1646
Number of pages11
JournalJournal of General Virology
Issue numberPART7
Publication statusPublished - 2013 Jul 1


ASJC Scopus subject areas

  • Virology

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