Linked Life Data

15107989

Source:http://linkedlifedata.com/resource/pubmed/id/15107989

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2005-4-27
pubmed:abstractText
The 2-5A/RNase L pathway belongs to the antiviral system induced by interferon (IFN). RNase L is an inactive endoribonuclease which is activated by 2'-5' oligoadenylate (2-5A) synthesized by 2',5'-oligoadenylate synthetases. Once activated, RNase L cleaves mRNA, inhibiting the protein synthesis, as well as 28S and 18S ribosomal RNA (rRNA), leading to ribosomal inactivation. In this study, we investigate the role of the RNase L pathway as a cell defence mechanism during Varicella-zoster virus (VZV) replication, and the importance of a 68-kDa protein named RNase L inhibitor (RLI), which specifically inhibits RNase L. We demonstrate that the RNase L and RLI transcripts levels remain constant in VZV-infected cells for 24 h and 12 h, respectively, after which they decrease until the end of the viral cycle. VZV does not significantly modulate the protein level of RNase L during the course of infection. Using an rRNA cleavage assay to analyse the RNase L catalytic activity, we demonstrate that VZV replication leads to a minimal cleavage of rRNA. Moreover, the overexpression of RLI in a permissive cell line has no significant effect on the VZV replication. We conclude that RNase L does not constitute a major cell defence mechanism against the VZV infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0300-8584
pubmed:author
pubmed:issnType
Print
pubmed:volume
194
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-31
pubmed:dateRevised
2011-6-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Varicella-zoster virus does not significantly induce cell defence mechanism mediated by the 2-5A/RNase L pathway during its replication cycle.
pubmed:affiliation
University of Witten/Herdecke, Institute of Microbiology and Virology, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't