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Author Danaher, Robert J. ♦ Jacob, Robert J. ♦ Steiner, Marion R. ♦ Allen, Will R. ♦ Hill, James M. ♦ Miller, Craig S.
Source SpringerLink
Content type Text
Publisher Springer-Verlag
File Format PDF
Copyright Year ©2005
Language English
Subject Domain (in DDC) Technology ♦ Medicine & health
Subject Keyword herpes simplex virus ♦ histone deacetylase inhibitor ♦ latency-associated transcript ♦ PC12 cells ♦ quiescence ♦ reactivation ♦ Neurosciences ♦ Virology ♦ Infectious Diseases ♦ Immunology ♦ Neurology
Abstract Histone acetylation is implicated in the regulation of herpes simplex virus type 1 (HSV-1) latency. However, the role of histone acetylation in HSV-1 reactivation is less clear. In this study, the well-established model system, quiescently infected, neuronally differentiated PC12 (QIF-PC12) cells, was used to address the participation of histone acetylation in HSV-1 reactivation. In this model, sodium butyrate and trichostatin A (TSA), two histone deacetylase inhibitors, stimulated production of infectious HSV-1 progeny from a quiescent state. To identify viral genes responsive to TSA, the authors analyzed representative α, β, and γ viral genes using quantitative real-time polymerase chain reaction. Only the latency-associated transcript (LAT) accumulated in response to TSA treatment, under culture conditions that restricted virus replication and spread. This led the authors to evaluate the importance of LAT expression on TSA-induced reactivation. In QIF-PC12 cells, the LAT deletion mutant virus dLAT2903 reactivated equivalently with its wild-type parental strain (McKrae) after TSA treatment, as well as forskolin and heat stress treatment. Both viruses also reactivated equivalently from latently infected trigeminal ganglia explants from rabbits. In contrast, there was a marked reduction in the recovery of dLAT2903, as compared to wild-type virus, from the eyes of latently infected rabbits following epinephrine iontophoresis. These combined in vitro, ex vivo, and in vivo data suggest that LAT is not required for reactivation from latently infected neuronal cells per se, but may enhance processes that allow for the arrival of virus at, or close to, the site of original inoculation (i.e., recrudescence).
ISSN 13550284
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG
Learning Resource Type Article
Publisher Date 2005-01-01
Publisher Place New York
e-ISSN 15382443
Journal Journal of NeuroVirology
Volume Number 11
Issue Number 3
Page Count 12
Starting Page 306
Ending Page 317

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Source: SpringerLink