MOLECULAR ANALYSIS OF HERPES-SIMPLEX VIRUS TYPE-1 DURING EPINEPHRINE-INDUCED REACTIVATION OF LATENTLY INFECTED-RABBITS IN-VIVO

被引:122
|
作者
BLOOM, DC
DEVIRAO, GB
HILL, JM
STEVENS, JG
WAGNER, EK
机构
[1] UNIV CALIF IRVINE, DEPT MOLEC BIOL & BIOCHEM, IRVINE, CA 92717 USA
[2] UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, LOS ANGELES, CA 90024 USA
[3] LOUISIANA STATE UNIV, MED CTR, CTR EYE, LIONS EYE RES LABS, NEW ORLEANS, LA 70112 USA
关键词
D O I
10.1128/JVI.68.3.1283-1292.1994
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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,vith 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.
引用
收藏
页码:1283 / 1292
页数:10
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