ArticleMedical microbiology and immunology2005
Varicella-zoster virus does not significantly induce cell defence mechanism mediated by the 2-5A/RNase L pathway during its replication cycle.
Article in Medical microbiology and immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- Transcriptional response to VZV infection is modulated by RNA polymerase III in lung epithelial cell lines.Frontiers in cellular and infection microbiology · 2022Article
- Specific inhibition of the PKR-mediated antiviral response by the murine cytomegalovirus proteins m142 and m143.Journal of virology · 2009Article
- ICP0 prevents RNase L-independent rRNA cleavage in herpes simplex virus type 1-infected cells.Journal of virology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.