Axin expression delays herpes simplex virus-induced autophagy and enhances viral replication in L929 cells

Eun Jin Choi, Sun Ho Kee

Research output: Contribution to journalArticle

4 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)103-111
Number of pages9
JournalMicrobiology and Immunology
Volume58
Issue number2
DOIs
Publication statusPublished - 2014 Feb

Keywords

  • Autophagy
  • Axin
  • Herpes simplex virus

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Virology

Fingerprint Dive into the research topics of 'Axin expression delays herpes simplex virus-induced autophagy and enhances viral replication in L929 cells'. Together they form a unique fingerprint.

  • Cite this