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Journal of Virology, March 2000, p. 2603-2611, Vol. 74, No. 6
Institute for Animal Health, Pirbright,
Surrey GU24 ONF, United Kingdom
Received 20 August 1999/Accepted 21 December 1999
Rinderpest virus is a morbillivirus and the causative
agent of an important disease of cattle and wild bovids. The P genes of
all morbilliviruses give rise to two proteins in addition to the P
protein itself: use of an alternate start translation site, in a second
open reading frame, gives rise to the C protein, while cotranscriptional insertion of an extra base gives rise to the V
protein, a fusion of the amino-terminal half of P to a short, highly
conserved, cysteine-rich zinc binding domain. Little is known about the
function of either of these two proteins in the rinderpest virus life
cycle. We have constructed recombinant rinderpest viruses in which the
expression of these proteins has been suppressed, individually and
together, and studied the replication of these viruses in tissue
culture. We show that the absence of the V protein has little effect on
the replication rate of the virus but does lead to an increase in
synthesis of genome and antigenome RNAs and a change in cytopathic
effect to a more syncytium-forming phenotype. Virus that does not
express the C protein, on the other hand, is clearly defective in
growth in all cell lines tested, and this defect appears to be related
to a decreased transcription of mRNA from viral genes. The phenotypes
of both individual mutant virus types are both expressed in the double
mutant expressing neither V nor C.
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Rinderpest Viruses Lacking the C and V Proteins
Show Specific Defects in Growth and Transcription of Viral
RNAs
*
Corresponding author. Mailing address: Institute for
Animal Health, Ash Road, Pirbright, Surrey GU24 ONF, United Kingdom. Phone: 44 (0) 1483 232441. Fax: 44 (0) 1483 232448. E-mail:
michael.baron{at}bbsrc.ac.uk.
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