The US 9, 10, 11, and 12 genes of herpes simplex virus type 1 are of no importance for its neurovirulence and latency in mice.
We have studied the pathogenic and latency/reactivation potential of a herpes simplex virus type 1 (HSV-1) variant (N38) which has a deletion of four genes, US9, US10, US11, and US12, in the short unique region of the HSV-1 genome. N38 was as pathogenic as the parental wild-type virus following intracerebral infection of mice and replicated with wild-type kinetics in the brain. After intraperitoneal infection, some restricted replication of N38 was observed in the adrenal gland and the deletion virus was about 20-fold less virulent than the parental virus. There was no significant difference between two viruses in the frequency of reactivation or in reactivation time. The results indicate that US9, US10, US11, and US12 gene products are dispensable for its neurovirulence and latency in mice.
Nishiyama
Y
Y
Laboratory of Virology, Nagoya University School of Medicine, Japan.
Kurachi
R
R
Daikoku
T
T
Umene
K
K
D000818:Animals; D001921:Brain / Q000382:microbiology; D003315:Cornea / Q000382:microbiology; D017353:Gene Deletion; D005814:Genes, Viral / Q000235:genetics*; D014644:Genetic Variation; D016679:Genome, Viral; D007928:Lethal Dose 50; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009928:Organ Specificity; D016601:RNA-Binding Proteins / Q000235:genetics; D018139:Simplexvirus / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity*; D014764:Viral Proteins / Q000235:genetics*; D014774:Virulence
D016601:RNA-Binding Proteins; C074546:US11 protein, herpesvirus; D014764:Viral Proteins