Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1A
pubmed:dateCreated
1982-9-10
pubmed:abstractText
Acyclovir [9-(2-hydroxyethoxymethyl)guanine] inhibits Epstein-Barr virus (EBV) replication in lymphoblastoid cells at concentrations nontoxic to cellular growth. The mode of action of the drug against EBV differs from the mechanism described in herpes simplex virus systems. Due to the absence of virus-specified thymidine kinase, the drug is poorly phosphorylated in EBV-infected cells. The extent of monophosphorylation is similar both in mock-infected and EBV-infected cells. Despite weak phosphorylation of the drug, the replication of linear EBV DNA is inhibited due to exquisite sensitivity of the viral DNA polymerase. Activation of acyclovir does not require phosphorylation by virus-specified thymidine kinase, inhibition of different herpes-group viruses depends on three variable factors: degree of phosphorylation, cellular metabolism of the drug, and degree of sensitivity of the viral polymerase. Interaction of acyclovir-triphosphate with EBV DNA polymerase is reversible. Cells infected with EBV and treated with acyclovir resume virus replication following removal of the drug even after long exposure. Acyclovir inhibits replication of linear genomes and stops production of virus, but has no effect on latent cellular infection. These results lead us to predict that acyclovir will suppress, but not cure, EBV infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0002-9343
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
18-26
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Perspectives on interactions of acyclovir with Epstein-Barr and other herpes viruses.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't