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

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.

journal_name

J Virol

journal_title

Journal of virology

authors

Chen LL,Kung YA,Weng KF,Lin JY,Horng JT,Shih SR

doi

10.1128/JVI.02278-12

subject

Has Abstract

pub_date

2013-04-01 00:00:00

pages

3828-38

issue

7

eissn

0022-538X

issn

1098-5514

pii

JVI.02278-12

journal_volume

87

pub_type

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