Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-4-3
pubmed:abstractText
We previously showed that the LAT function required for efficient spontaneous reactivation of herpes simplex virus type 1 (HSV-1) from neuronal latency in the rabbit maps within the first 1.5 kb of the 8.3-kb primary LAT transcript. This demonstrated that LAT does not function via an antisense mechanism, since the first 1.5 kb of LAT does not overlap any other known HSV-1 gene. Furthermore, if LAT encodes a protein essential for efficient spontaneous reactivation, it must map within the functional first 1.5 kb of LAT. Thus, the absence of a well-conserved LAT open reading frame in this region among all HSV-1 LAT genes capable of supporting high levels of spontaneous reactivation would demonstrate that LAT does not encode a protein essential for efficient spontaneous reactivation. In this report, we sequenced the first 1.5 kb of LAT from HSV-1 McKrae, a strain with a very high spontaneous reactivation rate. Of the HSV-1 LAT sequences available for comparison (17syn+, KOS, and F), only strain 17syn+ has a high spontaneous reactivation rate. However, as shown in this report, a chimeric virus containing the KOS LAT gene on an HSV-1 McKrae genetic background had a spontaneous reactivation rate indistinguishable from McKrae (15 versus 13.6%; P > 0.05). Thus, the spontaneous reactivation competency of the LAT gene from HSV-1 KOS was similar to that of the McKrae LAT gene. Comparative sequence analysis of the LAT genes from McKrae, 17syn+, and KOS revealed that none of the eight potential McKrae LAT ORFs were well conserved. Additional types of sequence analyses further confirmed that none of the potential ORFs were likely to encode a functional LAT protein. These results strongly support the notion that the LAT function involved in spontaneous reactivation is mediated by a direct DNA or RNA mechanism rather than a protein.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
242
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
221-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9501054-Animals, pubmed-meshheading:9501054-Base Sequence, pubmed-meshheading:9501054-Conserved Sequence, pubmed-meshheading:9501054-Eye, pubmed-meshheading:9501054-Genes, Viral, pubmed-meshheading:9501054-Herpes Simplex, pubmed-meshheading:9501054-Herpesvirus 1, Human, pubmed-meshheading:9501054-Kinetics, pubmed-meshheading:9501054-Molecular Sequence Data, pubmed-meshheading:9501054-Neurons, pubmed-meshheading:9501054-Open Reading Frames, pubmed-meshheading:9501054-Rabbits, pubmed-meshheading:9501054-Sequence Alignment, pubmed-meshheading:9501054-Sequence Homology, Nucleic Acid, pubmed-meshheading:9501054-Transcription, Genetic, pubmed-meshheading:9501054-Virulence, pubmed-meshheading:9501054-Virus Activation, pubmed-meshheading:9501054-Virus Latency, pubmed-meshheading:9501054-Virus Replication
pubmed:year
1998
pubmed:articleTitle
The region of the herpes simplex virus type 1 LAT gene involved in spontaneous reactivation does not encode a functional protein.
pubmed:affiliation
Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns and Allen Research Institute, Los Angeles, California 90048, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't