Journal
VIRUS RESEARCH
Volume 208, Issue -, Pages 22-29Publisher
ELSEVIER
DOI: 10.1016/j.virusres.2015.05.020
Keywords
Coxsackievirus B3; 2A protease; EMCV; IRES; Protein translation
Categories
Funding
- China Mega-Project for Infectious Disease [2011ZX10004-001, 2012ZX10004215, 2013ZX10004805002]
- National Natural Science Foundation of China [31371397]
- Beijing Natural Science Foundation [7144197]
- SKLID Development Grant [2011SKLID104]
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To determine whether 2A protease of the enterovirus genus with type I internal ribosome entry site (IRES) effect on the viral replication of type II IRES, coxsackievirus B3(CVB3)-encoded protease 2A and encephalomyocarditis virus (EMCV) IRES (Type II)-dependent or cap-dependent report gene were transiently co-expressed in eukaryotic cells. We found that CVB3 2A protease not only inhibited translation of cap-dependent reporter genes through the cleavage of eIF4GI, but also conferred high EMCV IRES-dependent translation ability and promoted EMCV replication. Moreover, deletions of short motif (aa13-18 RVVNRH, aa65-70 KNKHYP, or aa88-93 PRRYQSH) resembling the nuclear localization signals (NLS) or COOH-terminal acidic amino acid motif (aa133-147 DIRDLLWLEDDAMEQ) of CVB3 2A protease decreased both its EMCVIRES-dependent translation efficiency and destroy its cleavage on eukaryotic initiation factor 4G (eIF4G) I. Our results may provide better understanding into more effective interventions and treatments for co-infection of viral diseases. (C) 2015 Elsevier B.V. All rights reserved.
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