Regulation of human parainfluenza virus type 3 fusion protein expression
| dc.contributor.author | Murphy, Lise | |
| dc.date.accessioned | 2013-11-07T17:25:45Z | |
| dc.date.available | 2013-11-07T17:25:45Z | |
| dc.date.created | 2004 | |
| dc.date.issued | 2004 | |
| dc.degree.level | Masters | |
| dc.degree.name | M.Sc. | |
| dc.description.abstract | Human parainfluenza virus type 3 (HPIV3) is an enveloped, negative-strand, non-segmented RNA virus. HPIV3 is a human respiratory pathogen that primarily causes diseases such as croup, bronchiolitis and pneumonia in children. The virus has two glycoproteins that allow it to interact with host cells, the receptor binding protein hemagglutinin-neuraminidase (HN) and the fusion protein (F), which enables the virus to enter the cell by fusion of the viral envelope to the target cell plasma membrane. This research was initiated with the goal of determining mechanisms by which HPIV3 regulates the expression of the fusion protein. Evidence indicated that the transcription of the F gene differed from that of the other genes because there was a very high level of read-through transcription at the junction of the matrix (M) gene and the F gene. This read-through transcription caused >80% of the potential F gene transcripts to be present in biscistronic M/F mRNA, in which the F open reading frame cannot be translated. (Abstract shortened by UMI.) | |
| dc.format.extent | 89 p. | |
| dc.identifier.citation | Source: Masters Abstracts International, Volume: 43-06, page: 2095. | |
| dc.identifier.uri | http://hdl.handle.net/10393/26723 | |
| dc.identifier.uri | http://dx.doi.org/10.20381/ruor-18338 | |
| dc.language.iso | en | |
| dc.publisher | University of Ottawa (Canada) | |
| dc.subject.classification | Biology, Microbiology. | |
| dc.subject.classification | Chemistry, Biochemistry. | |
| dc.subject.classification | Health Sciences, Public Health. | |
| dc.title | Regulation of human parainfluenza virus type 3 fusion protein expression | |
| dc.type | Thesis |
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