Sequence analysis of the herpes simplex virus type 1 strain 17 variants 1704, 1705 and 1706 with respect to their origin and effect on the latency-associated transcript sequence.
The precise endpoints of the deletions/insertions in three variants (1704, 1705 and 1706) of herpes simplex virus type 1 (HSV-1) strain 17 have been determined by dideoxynucleotide sequence analysis. The analysis was undertaken to discover whether the three variants had arisen from the same initial event and the extent of the deletions with respect to the latency-associated transcripts (LATs) and the proposed LAT promoter region. It is not possible from the deletion boundaries to determine unequivocally whether the three variants had arisen from the same recombination event although 1706 could be descended from 1705 by illegitimate recombination. The results demonstrate that spontaneous deletions can occur at random within RL, the extent of the deletions in UL is constrained by the essential nature of UL genes in vitro but is otherwise arbitrary and deletions in 1704 completely remove both copies of the LAT promoter region and in IRL extend into the 5' end of the LAT sequence.
Junejo
F
F
MRC Virology Unit, Institute of Virology, Glasgow, U.K.
MacLean
A R
AR
Brown
S M
SM
D015139:Blotting, Southern; D003001:Cloning, Molecular; D004279:DNA, Viral / Q000032:analysis*; D006801:Humans; D016296:Mutagenesis; D016254:Mutagenesis, Insertional; D009693:Nucleic Acid Hybridization; D015345:Oligonucleotide Probes; D011401:Promoter Regions, Genetic; D011995:Recombination, Genetic; D012091:Repetitive Sequences, Nucleic Acid; D015183:Restriction Mapping; D018139:Simplexvirus / Q000235:genetics*; D014158:Transcription, Genetic
D004279:DNA, Viral; D015345:Oligonucleotide Probes