Abstract |
In this report we have monitored viral gene expression, both at the RNA and protein level, after the establishment of a long-term persistent infection of Sendai virus. The persistent infection was initially established by infecting BHK cells with a viral stock containing a short (1.4 kb) copy-back DI (DIH4). After over 120 weeks in culture this short copy-back DI had been replaced by two large deletion DIs (approximately 7 and 12 kb) from which was expressed an N-terminally truncated form of the P protein. The mRNA for this protein was detected in cells and the deletion within the P gene was mapped by PCR cloning and sequencing of intracellular nucleocapsid RNA. This truncated P protein (derived by deleting the N-terminal half of the cloned Pwt gene) has already been shown to function as a dominant negative for DI replication when driven by cloned viral genes. Cloning and expression of the truncated P from the long-term persistent infection revealed that this protein had retained the dominant negative phenotype. The presence of such a protein would severely depress viral gene expression and may therefore play an important role in the maintenance of persistence.
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Authors | D Garcin, M De Melo, L Roux, D Kolakofsky, J Curran |
Journal | Virology
(Virology)
Vol. 201
Issue 1
Pg. 19-25
(May 15 1994)
ISSN: 0042-6822 [Print] United States |
PMID | 8178486
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- P protein, Sendai virus
- Phosphoproteins
- RNA, Viral
- Viral Proteins
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Topics |
- Animals
- Base Sequence
- Cell Line
- Cloning, Molecular
- Cricetinae
- Defective Viruses
(physiology)
- Gene Expression Regulation, Viral
(genetics)
- Genes, Dominant
- Genes, Viral
(genetics)
- Molecular Sequence Data
- Parainfluenza Virus 1, Human
(physiology)
- Phosphoproteins
(analysis, genetics, physiology)
- RNA, Viral
(analysis)
- Viral Proteins
(analysis, genetics, physiology)
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