Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1997-9-17
pubmed:abstractText
In this study we used a herpes simplex virus type 1 (HSV-1) deletion mutant to identify a segment of the genome necessary for epinephrine-induced reactivation in the rabbit eye model of herpetic recurrent disease. In HSV-1 latently infected neural tissue, the only abundant viral products are the latency-associated transcripts (LATs). At least one promoter of LAT has been identified, and mutations in the LAT domain have been used to investigate HSV-1 reactivation. We used an ocular rabbit model of epinephrine-induced HSV-1 reactivation to study the effects of deleting a 437-bp region beginning 796 bp upstream of the LAT CAP site. Specifically, the 437-bp deletion is located between genomic positions 118006 and 118443 of the parent 17Syn+, and the construct is designated 17 delta S/N. This region also controls a portion of the genome encoding two transcripts (1.1 and 1.8 kb) from the LAT domain. A rescuant, 17 delta S/N-Res, was constructed from 17 delta S/N. Following ocular infection, all three viruses produced similar acute dendritic lesions in rabbits. Five weeks after infection, rabbits received transcorneal iontophoresis of epinephrine. The parent, 17Syn+, and the rescuant, 17 delta S/N-Res, underwent a high frequency of HSV-1 ocular reactivation as determined by recovery of infectious virus in the tear film. Rabbits infected with 17 delta S/N had a significantly lower frequency of ocular reactivation. Analysis of the trigeminal ganglia from all three groups of latently infected rabbits revealed (i) similar amounts of HSV DNA (genomic equivalents), (ii) accumulation of 2.0- and 1.45-kb LATs, and (iii) explant reactivation at the same high frequency. Therefore, these studies indicate that the 437-bp deleted region in 17 delta S/N is essential for epinephrine-induced reactivation and could implicate the 1.1- and 1.8-kb transcripts in the mechanisms controlling HSV-1 reactivation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-1658388, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-2152989, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-2161947, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-3009094, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-3030660, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-3117494, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-7966571, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-7966594, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8107194, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8151759, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8313476, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8380666, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8388517, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8395115, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8551638, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8627728, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8627793, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8642650, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8709218, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8794381, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8799218, http://linkedlifedata.com/resource/pubmed/commentcorrection/9261376-8850545
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-538X
pubmed:author
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6555-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:9261376-Adrenergic Agonists, pubmed-meshheading:9261376-Animals, pubmed-meshheading:9261376-Base Composition, pubmed-meshheading:9261376-Blotting, Southern, pubmed-meshheading:9261376-Cell Line, pubmed-meshheading:9261376-Cercopithecus aethiops, pubmed-meshheading:9261376-Cornea, pubmed-meshheading:9261376-DNA, Viral, pubmed-meshheading:9261376-Epinephrine, pubmed-meshheading:9261376-Genotype, pubmed-meshheading:9261376-Herpesvirus 1, Human, pubmed-meshheading:9261376-Humans, pubmed-meshheading:9261376-Keratitis, Herpetic, pubmed-meshheading:9261376-Promoter Regions, Genetic, pubmed-meshheading:9261376-Rabbits, pubmed-meshheading:9261376-Sequence Deletion, pubmed-meshheading:9261376-Trigeminal Ganglion, pubmed-meshheading:9261376-Vero Cells, pubmed-meshheading:9261376-Virus Activation, pubmed-meshheading:9261376-Virus Latency
pubmed:year
1997
pubmed:articleTitle
A 437-base-pair deletion at the beginning of the latency-associated transcript promoter significantly reduced adrenergically induced herpes simplex virus type 1 ocular reactivation in latently infected rabbits.
pubmed:affiliation
LSU Eye Center, Louisiana State University School of Medicine, New Orleans 70112-2234, USA. JHILL@LSUMC.EDU
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.