Herpes simplex virus type 1 deletion variants 1714 and 1716 pinpoint neurovirulence-related sequences in Glasgow strain 17+ between immediate early gene 1 and the 'a' sequence.

摘要: Dideoxynucleotide sequence analysis of a spontaneously isolated deletion variant (1714) Glasgow strain 17+ herpes simplex virus type 1 (HSV-1) demonstrates that the is 759 bp in length and located within each copy BamHI s fragment (0 to 0.02 0.81 0.83 map units) long repeat region genome. The removes one complete 18 DR1 element ‘a’ terminates 1105 upstream 5′ end immediate early (IE) gene 1. grows high titre, not temperature-sensitive host cell type-restricted vitro. In vivo studies demonstrate 1714 totally avirulent for BALB/c mice following intracerebral inoculation, with an LD50 7 × 106 p.f.u./mouse compared < 10 parental wild-type 17+. growth kinetics show non-neurovirulent phenotype due inability replicate mouse brain. Because was genomic background which four XbaI sites had been removed because thymidine kinase-negative, introduced into otherwise background. resulting (1716) nonneurovirulent mice, p.f.u./mouse. does prevent from establishing latent infection or reactivating it results sequences between IE-1 produce neurovirulence and, conjunction nonneurovirulence HSV-2 HG52 JH2604, identify common function conserved HSV-1 -2.