Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-12-15
pubmed:abstractText
We have previously found that interleukin (IL)-2, IL-10, interferon (IFN)-gamma, RANTES, and tumor necrosis factor (TNF)-alpha mRNA transcription remain elevated in the trigeminal ganglia (TG) of herpes simplex virus type 1 (HSV-1) latently infected mice up to 120 days postinoculation (p.i.). To determine if this phenomenon was dependent on HSV-1 DNA replication after the establishment of latency (i.e., reactivation), cytokine gene expression was compared in TG of acyclovir-treated and untreated latently infected mice. Oral acyclovir treatment (begun 16 days p.i.) had no effect on serum levels of total anti-HSV-1 antibodies. However, there was a significant reduction in the titer of antibody specific for glycoprotein D and glycoprotein B but not glycoprotein H/L 120 days PI in the acyclovir-treated compared to vehicle-treated mice. These differences were not significant at earlier time points (i.e., days 34 and 60 p.i.). Consistent with these findings, acyclovir had no effect on cytokine gene expression in latently infected TG 35 and 60 days p.i. However, 120 days p.i., IFN-gamma and TNF-alpha mRNA were approaching baseline levels in TG of acyclovir-treated mice, but remained significantly elevated in untreated controls (i.e., IFN-gamma mRNA levels were sixfold higher in TG of untreated mice). Therefore, viral DNA replication appears to provide an antigenic stimulus for persistent cytokine gene expression in latently infected TG.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9375008-Acyclovir, pubmed-meshheading:9375008-Analysis of Variance, pubmed-meshheading:9375008-Animals, pubmed-meshheading:9375008-Antibodies, Viral, pubmed-meshheading:9375008-Antiviral Agents, pubmed-meshheading:9375008-Cell Line, pubmed-meshheading:9375008-Cercopithecus aethiops, pubmed-meshheading:9375008-Cytokines, pubmed-meshheading:9375008-DNA Primers, pubmed-meshheading:9375008-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:9375008-Gene Expression Regulation, pubmed-meshheading:9375008-Herpes Simplex, pubmed-meshheading:9375008-Herpesvirus 1, Human, pubmed-meshheading:9375008-Mice, pubmed-meshheading:9375008-Polymerase Chain Reaction, pubmed-meshheading:9375008-Transcription, Genetic, pubmed-meshheading:9375008-Trigeminal Ganglion, pubmed-meshheading:9375008-Virus Latency, pubmed-meshheading:9375008-Virus Replication
pubmed:year
1997
pubmed:articleTitle
Acyclovir blocks cytokine gene expression in trigeminal ganglia latently infected with herpes simplex virus type 1.
pubmed:affiliation
Department of Microbiology and Immunology, Louisiana State University Medical Center, New Orleans 70112-1393, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.