Enterovirus 71 infection cleaves a negative regulator for viral internal ribosomal entry site-driven translation.
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.
Research Center for Emerging Viral Infections, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Li-Lien
LL
Chen
Yu-An
YA
Kung
Kuo-Feng
KF
Weng
Jing-Yi
JY
Lin
Jim-Tong
JT
Horng
Shin-Ru
SR
Shih
D015153:Blotting, Western; D045744:Cell Line, Tumor; D029821:Enterovirus A, Human / Q000378:metabolism*; D004769:Enterovirus Infections / Q000378:metabolism*; D006801:Humans; D010957:Plasmids / Q000235:genetics; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D014176:Protein Biosynthesis / Q000502:physiology*; D034741:RNA, Small Interfering / Q000235:genetics; D016601:RNA-Binding Proteins / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism*; D053586:Virus Internalization; D014779:Virus Replication / Q000502:physiology
C105789:KHSRP protein, human; D034741:RNA, Small Interfering; D016601:RNA-Binding Proteins; D015534:Trans-Activators; D046988:Proteasome Endopeptidase Complex