Linked Life Data

15670795

Source:http://linkedlifedata.com/resource/pubmed/id/15670795

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-26
pubmed:abstractText
The present study investigated the role of interferon-inducible pathways in herpes simplex virus type 1-infected mice transduced with an adenoviral vector expressing murine interferon-beta (Ad:IFN-beta). Wild type mice or RNase L(-/-) mice deficient in responses to 2'-5' oligoadenylate synthetase activation, or lacking RNA-dependent protein kinase and transduced with Ad:IFN-beta showed enhanced survival following HSV-1 infection. The protective effect was associated with a reduction in viral gene expression in the cornea and trigeminal ganglion in wild type mice as well as the trigeminal ganglion of RNase L(-/-) mice. However, the efficacy of Ad:IFN-beta was lost in the corneas of RNase L(-/-) mice and significantly diminished in both the cornea and trigeminal ganglion as measured by viral gene expression in RNA-dependent protein kinase deficient mice. Collectively, the data suggest survival rates of viral-infected mice do not reflect the replication capacity as measured by herpes simplex virus type one lytic gene expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-4835
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
167-73
pubmed:dateRevised
2011-6-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Dichotomy between survival and lytic gene expression in RNase L- and PKR-deficient mice transduced with an adenoviral vector expressing murine IFN-beta following ocular HSV-1 infection.
pubmed:affiliation
Department of Ophthalmology, Microbiology, and Immunology, University of Oklahoma Health Sciences Center, HSC608 Stanton L Young Blvd, Oklahoma City, OK 73104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't