Linked Life Data

8386887

Source:http://linkedlifedata.com/resource/pubmed/id/8386887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-5-27
pubmed:abstractText
We have studied the pathogenic and latency/reactivation potential of a herpes simplex virus type 1 (HSV-1) variant (N38) which has a deletion of four genes, US9, US10, US11, and US12, in the short unique region of the HSV-1 genome. N38 was as pathogenic as the parental wild-type virus following intracerebral infection of mice and replicated with wild-type kinetics in the brain. After intraperitoneal infection, some restricted replication of N38 was observed in the adrenal gland and the deletion virus was about 20-fold less virulent than the parental virus. There was no significant difference between two viruses in the frequency of reactivation or in reactivation time. The results indicate that US9, US10, US11, and US12 gene products are dispensable for its neurovirulence and latency in mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:volume
194
pubmed:geneSymbol
US10, US11, US12, US9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
419-23
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
The US 9, 10, 11, and 12 genes of herpes simplex virus type 1 are of no importance for its neurovirulence and latency in mice.
pubmed:affiliation
Laboratory of Virology, Nagoya University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't