Replication-competent foot-and-mouth disease virus RNAs lacking capsid coding sequences
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Replication-competent foot-and-mouth disease virus RNAs lacking capsid coding sequences. / McInerney, Gerald M.; King, Andrew M.Q.; Ross-Smith, Natalie; Belsham, Graham J.
I: Journal of General Virology, Bind 81, Nr. 7, 2000, s. 1699-1702.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Replication-competent foot-and-mouth disease virus RNAs lacking capsid coding sequences
AU - McInerney, Gerald M.
AU - King, Andrew M.Q.
AU - Ross-Smith, Natalie
AU - Belsham, Graham J.
PY - 2000
Y1 - 2000
N2 - RNA transcripts were prepared from plasmids encoding an infectious cDNA of foot-and-mouth disease virus (FMDV) or derivatives in which the leader (Lab and Lb) and capsid protein coding sequences were deleted or replaced by sequences encoding chloramphenicol acetyltransferase (CAT). The transcripts were electroporated into BHK cells and the expression of CAT and the FMDV 3C protease was monitored. Detection of CAT and 3C was dependent on the ability of the transcript to replicate. All of the Lb coding sequence and 94% of P1 (the capsid protein precursor) coding sequence could be deleted without any apparent effect on the ability of the RNA to replicate. Thus, no cis-acting replication element is present within this region of the FMDV genome. Trans-encapsidation of these FMDV replicons was very inefficient, which may explain the lack of production of defective-interfering particles in FMDV-infected cells.
AB - RNA transcripts were prepared from plasmids encoding an infectious cDNA of foot-and-mouth disease virus (FMDV) or derivatives in which the leader (Lab and Lb) and capsid protein coding sequences were deleted or replaced by sequences encoding chloramphenicol acetyltransferase (CAT). The transcripts were electroporated into BHK cells and the expression of CAT and the FMDV 3C protease was monitored. Detection of CAT and 3C was dependent on the ability of the transcript to replicate. All of the Lb coding sequence and 94% of P1 (the capsid protein precursor) coding sequence could be deleted without any apparent effect on the ability of the RNA to replicate. Thus, no cis-acting replication element is present within this region of the FMDV genome. Trans-encapsidation of these FMDV replicons was very inefficient, which may explain the lack of production of defective-interfering particles in FMDV-infected cells.
UR - http://www.scopus.com/inward/record.url?scp=0033947728&partnerID=8YFLogxK
U2 - 10.1099/0022-1317-81-7-1699
DO - 10.1099/0022-1317-81-7-1699
M3 - Journal article
C2 - 10859374
AN - SCOPUS:0033947728
VL - 81
SP - 1699
EP - 1702
JO - Journal of General Virology
JF - Journal of General Virology
SN - 0022-1317
IS - 7
ER -
ID: 379027849