An HSV-1 containing the rat beta-glucuronidase cDNA inserted within the LAT gene is less efficient than the parental strain at establishing a transcriptionally active state during latency in neurons.
Gene Ther
; 2(3): 209-17, 1995 May.
Article
en En
| MEDLINE
| ID: mdl-7614252
ABSTRACT
The herpes simplex virus vector 17/LAT-RGUSB has previously been shown to express beta-glucuronidase enzyme activity stably in the trigeminal ganglia and brain stems of beta-glucuronidase-deficient mutant mice. However, the number of beta-glucuronidase expressing cells in trigeminal ganglia latently infected with 17/LAT-RGUSB was smaller than expected. Using normal mice for further characterization of 17/LAT-RGUSB latent infection, no appreciable differences were found between the vector and wild-type virus in (1) their abilities to replicate in acutely infected ganglia; (2) their abilities to reactivate from latently infected ganglia or (3) the quantities of viral DNA in tissues during the acute or the latent phases of infection. Using a minor LAT (mLAT)-specific probe to detect transcription by in situ hybridization, it was found that the intensity of the signal from individual cells latently-infected with 17/LAT-RGUSB or wild-type virus was similar. However, the vector-infected ganglia had only 20% as many positive cells as in wild-type infection. These data suggest that 17/LAT-RGUSB virus established latency similarly to wild-type virus, but that the LAT-promoter driven gene expression was compromised.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Latencia del Virus
/
Herpesvirus Humano 1
/
Genes Virales
/
Vectores Genéticos
/
Glucuronidasa
/
Neuronas
Límite:
Animals
Idioma:
En
Revista:
Gene Ther
Asunto de la revista:
GENETICA MEDICA
/
TERAPEUTICA
Año:
1995
Tipo del documento:
Article
País de afiliación:
Estados Unidos