Molecular analysis of herpes simplex virus type 1 during epinephrine-induced reactivation of latently infected rabbits in vivo.
AUTOR(ES)
Bloom, D C
RESUMO
Infectious virus assays and PCR amplification of DNA and RNA were used to investigate herpes simplex virus (HSV) DNA replication and gene expression in the rabbit corneal model for virus reactivation in vivo. We used carefully defined latency-associated transcript-negative (LAT-) and LAT+ promoter mutants of the 17syn+ strain of HSV type 1. In agreement with earlier studies using a more extensive LAT- deletion mutant, the 17 delta Pst(LAT-) virus reactivated with extremely low frequency upon epinephrine induction. In contrast to our findings with murine latency models, amounts of viral DNA recovered from rabbit ganglia latently infected with either LAT+ or LAT- virus were equivalent. Also in contrast with the murine models, no net increase in viral DNA was seen in latently infected rabbit trigeminal ganglia induced to reactivate in vivo by iontophoresis of epinephrine. Despite this, transcription of lytic-phase genes could be detected within 4 h following induction of rabbits latently infected with either LAT+ or LAT- virus; this transcription diminished by 16 h following induction. These results are discussed in relation to models for the mechanism of action of HSV LAT.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=236581Documentos Relacionados
- Epinephrine-induced Insulin Resistance in Man
- Herpes simplex virus type 1 DNA replication and gene expression during explant-induced reactivation of latently infected murine sensory ganglia.
- The Probability of In Vivo Reactivation of Herpes Simplex Virus Type 1 Increases with the Number of Latently Infected Neurons in the Ganglia
- Rapid in vivo reactivation of herpes simplex virus in latently infected murine ganglionic neurons after transient hyperthermia.
- A 437-base-pair deletion at the beginning of the latency-associated transcript promoter significantly reduced adrenergically induced herpes simplex virus type 1 ocular reactivation in latently infected rabbits.