ArticleVirology journal2008
Varicella-zoster virus ORF 58 gene is dispensable for viral replication in cell culture.
Article in Virology journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Viral modulation of type II interferon increases T cell adhesion and virus spread.Nature communications · 2024Article
- Variable Gene Expression in Human Ganglia Latently Infected with Varicella-Zoster Virus.Viruses · 2022Article
- Herpesvirus BACs: past, present, and future.Journal of biomedicine & biotechnology · 2011Review
- Genome-wide mutagenesis reveals that ORF7 is a novel VZV skin-tropic factor.PLoS pathogens · 2010Article
- The varicella-zoster virus genome.Current topics in microbiology and immunology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOpen reading frame 58 (ORF58) of varicella-zoster virus (VZV) lies at the 3'end of the Unique long (UL) region and its functional is unknown. In order to clarify whether ORF58 is essential for the growth of VZV, we constructed a deletion mutant of ORF58 (pOka-BACDelta58) from the Oka parental genome cloned into a bacterial artificial chromosome (pOka-BAC).
resultsThe ORF58-deleted virus (rpOkaDelta58) was reconstituted from the pOka-BACDelta58 genome in MRC-5 cells, indicating that the ORF58 gene is non-essential for virus growth. Comparison of the growth rate of rpOkaDelta58 and recombinant wild-type virus by assessing plaque sizes revealed no significant differences between them both in MRC-5 cells and malignant melanoma cells.
conclusionThis study shows that the ORF58 gene is dispensable for viral replication and does not affect the virus' ability to form plaques in vitro.
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Registered trials
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