Dc. Bloom et al., MOLECULAR ANALYSIS OF HERPES-SIMPLEX VIRUS TYPE-1 DURING EPINEPHRINE-INDUCED REACTIVATION OF LATENTLY INFECTED-RABBITS IN-VIVO, Journal of virology, 68(3), 1994, pp. 1283-1292
Infectious virus assays and PCR amplification of DNA and RNA were used
to investigate herpes simplex virus (HSV) DNA replication and gene ex
pression in the rabbit corneal model for virus reactivation in vivo. W
e used carefully defined latency-associated transcript-negative (LAT(-
)) and LAT(+) promoter mutants of the 17syn(+) strain of HSV type 1. I
n agreement with earlier studies using a more extensive LAT(-) deletio
n mutant, the 17 Delta Pst(LAT(-)) virus reactivated with extremely lo
w frequency upon epinephrine induction. In contrast to our findings wi
th murine latency models, amounts of viral DNA recovered from rabbit g
anglia latently infected with either LAT(+) or LAT(-) virus were equiv
alent. Also in contrast with the murine models, no net increase in vir
al 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 follow
ing induction of rabbits latently infected,vith either LAT(+) or LAT(-
) virus; this transcription diminished by 16 h following induction. Th
ese results are discussed in relation to models for the mechanism of a
ction of HSV LAT.