Hazards from simian herpes viruses: reactivation of skin lesions with virus shedding.
Lancet
; 1(7908): 649-50, 1975 Mar 22.
Article
en En
| MEDLINE
| ID: mdl-47078
ABSTRACT
A new simian herpes virus with biological properties similar to herpes simplex and to simian "B" virus has been used as a model system for studying virus latency in dorsal root spinal sensory ganglia. Following intradermal injection, virus is present in the skin lesions and corresponding ganglia only, during the acute stage of the disease. By organ-culture techniques, latent virus was rescued from ganglia up to 2 years later. No latent virus was ever found in skin organ cultures of the primary site. Treatment with cortisone up to 18 months later reactivated virus latent in the ganglia, and virus returned to the skin where it produced small but typical herpes lesions which shed virus. Reactivation of Herpesvirus tamarinus was achieved after 28 months. This is believed to be the first report of a model system for the study of herpes latency in which skin lesions are found to recur, and provides an opportunity for more detailed investigations of the mechanisms of virus latency in man. The presumption that reactivation of skin lesions will also be possible in rhesus monkeys seropositive for "B" virus points to a possibly grave and largely unsuspected hazard for those engaged in primate research.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Piel
/
Infecciones por Herpesviridae
/
Herpesvirus Cercopitecino 1
/
Ganglios Espinales
/
Herpesviridae
Tipo de estudio:
Etiology_studies
/
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Lancet
Año:
1975
Tipo del documento:
Article