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Theiler’s murine encephalomyelitis virus contrasts with encephalomyocarditis and foot-and-mouth disease viruses in its functional utilization of the StopGo non-standard translation mechanism
Author(s) -
Gary Loughran,
Jane E. Libbey,
Sabena Uddowla,
Martina Scallan,
Martin D. Ryan,
Robert S. Fujinami,
Elizabeth Rieder,
John F. Atkins
Publication year - 2012
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/vir.0.047571-0
Subject(s) - biology , foot and mouth disease virus , virology , capsid , picornavirus , polyproteins , virus , aphthovirus , amino acid , genome , translation (biology) , encephalomyelitis , genetics , gene , immunology , messenger rna , multiple sclerosis
The picornaviruses' genome consists of a positive-sense ssRNA. Like many picornaviruses, cardioviruses synthesize two distinct polyprotein precursors from adjacent but non-overlapping genome segments. Both the [L-1ABCD-2A] and the [2BC-3ABCD] polyproteins are proteolytically processed to yield mature capsid and non-structural proteins, respectively. An unusual translational event, known as 'StopGo' or 'Stop-Carry on', is responsible for the release of the [L-1ABCD-2A] polyprotein from the ribosome and synthesis of the N-terminal amino acid of the [2BC-3ABCD] polyprotein. A common feature of these viruses is the presence of a highly conserved signature sequence for StopGo: -D(V/I)ExNPG(↓)P-, where -D(V/I)ExNPG are the last 7 aa of 2A, and the last P- is the first amino acid of 2B. Here, we report that, in contrast to encephalomyocarditis virus and foot-and-mouth disease virus, a functional StopGo does not appear to be essential for Theiler's murine encephalomyelitis virus viability when tested in vitro and in vivo.

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