Enterovirus 71 infection cleaves a negative regulator for viral internal ribosomal entry site-driven translation

Li Lien Chen, Yu An Kung, Kuo Feng Weng, Jing Yi Lin, Jim Tong Horng, Shin Ru Shih

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Far-upstream element-binding protein 2 (FBP2) is an internal ribosomal entry site (IRES) trans-acting factor (ITAF) that negatively regulates enterovirus 71 (EV71) translation. This study shows that EV71 infection cleaved FBP2. Live EV71 and the EV71 replicon (but not UV-inactivated virus particles) induced FBP2 cleavage, suggesting that viral replication results in FBP2 cleavage. The results also showed that virus-induced proteasome, autophagy, and caspase activity co-contribute to EV71-induced FBP2 cleavage. Using FLAG-fused FBP2, we mapped the potential cleavage fragments of FBP2 in infected cells. We also found that FBP2 altered its function when its carboxyl terminus was cleaved. This study presents a mechanism for virus-induced cellular events to cleave a negative regulator for viral IRES-driven translation.

Original languageEnglish
Pages (from-to)3828-3838
Number of pages11
JournalJournal of Virology
Volume87
Issue number7
DOIs
Publication statusPublished - Apr 2013
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Immunology
  • Virology

Cite this