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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2-3
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pubmed:dateCreated |
1995-2-2
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pubmed:abstractText |
In the present study we investigated the virulence and neural spread of pseudorabies virus (PRV) strains with mutations in the gene encoding glycoprotein I (gI) in 3-week-old pigs which were intranasally infected. Mutant M303 (lambda 125, 126) lacks amino acids valine-125 and cysteine-126 in an immunodominant antigenic region of gI which contains 2 discontinuous antigenic domains, whereas mutant virus M304 (lambda 59, 60) lacks amino acids glycine-59 and aspartic acid-60 in a continuous antigenic domain. Mutant M301 contains a frame shift mutation. Both mutants M301 (gI-) and M303 (lambda 125, 126) were not virulent for pigs, whereas mutant M304 (lambda 59, 60) was as virulent as wild-type PRV. All gI mutant viruses replicated in the oropharyngeal mucosa, although M304 (lambda 59, 60) and wild-type PRV replicated to higher titres than M303 (lambda 125, 126) and M301 (gI-). In contrast to M304 (lambda 59, 60) and wild-type PRV, both mutant viruses M301 (gI-) and M303 (lambda 125, 126) were not recovered from any part of the central nervous system at day 6 after infection. To study the spread of M301 (gI-) in the central nervous system in more detail, a second experiment was done in which 100-fold more virus was intranasally administered and virus was recovered from various tissues at day 4 after infection. Again, no gI-negative virus was isolated from the central nervous system. We concluded that deleting the amino acids valine-125 and cysteine-126 decreases virulence and reduces neurotropism to the same degree as deleting the gI protein. In addition, gI-negative virus does not spread in the central nervous system of pigs, probably because the transport of the virus across the synapse is hampered.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0236-6290
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
42
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
289-300
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7810422-Animals,
pubmed-meshheading:7810422-Brain,
pubmed-meshheading:7810422-Brain Diseases,
pubmed-meshheading:7810422-Cell Line,
pubmed-meshheading:7810422-Cells, Cultured,
pubmed-meshheading:7810422-Herpesvirus 1, Suid,
pubmed-meshheading:7810422-Kidney,
pubmed-meshheading:7810422-Mutation,
pubmed-meshheading:7810422-Oropharynx,
pubmed-meshheading:7810422-Pseudorabies,
pubmed-meshheading:7810422-Swine,
pubmed-meshheading:7810422-Swine Diseases,
pubmed-meshheading:7810422-Trigeminal Ganglion,
pubmed-meshheading:7810422-Viral Envelope Proteins,
pubmed-meshheading:7810422-Virulence,
pubmed-meshheading:7810422-Virus Replication
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pubmed:year |
1994
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pubmed:articleTitle |
Glycoprotein I of pseudorabies virus (Aujeszky's disease virus) determines virulence and facilitates penetration of the virus into the central nervous system of pigs.
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pubmed:affiliation |
Department of Virology, Central Veterinary Institute, Lelystad, The Netherlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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