ArticleJournal of virology2007
Deletion in open reading frame 49 of varicella-zoster virus reduces virus growth in human malignant melanoma cells but not in human embryonic fibroblasts.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 36 citations in OpenAlex.
- A human sensory neuron model for varicella-zoster virus latency and reactivationbioRxiv : the preprint server for biology · 2025Article
- Multi-proteomic profiling of the varicella-zoster virus-host interface reveals host susceptibilities to severe infection.Nature microbiology · 2025Article
- Article
- Features and Functions of the Conserved Herpesvirus Tegument Protein UL11 and Its Binding Partners.Frontiers in microbiology · 2022Review
- Article
- Article
- A spliced latency-associated VZV transcript maps antisense to the viral transactivator gene 61.Nature communications · 2018Article
- Varicella-zoster virus ORF49 functions in the efficient production of progeny virus through its interaction with essential tegument protein ORF44.Journal of virology · 2014Article
- A modified screening system for loss-of-function and dominant negative alleles of essential MCMV genes.PloS one · 2014Article
- BinAligner: a heuristic method to align biological networks.BMC bioinformatics · 2013Article
- Regulated interaction of tegument proteins UL16 and UL11 from herpes simplex virus.Journal of virology · 2012Article
- Interaction between the human cytomegalovirus tegument proteins UL94 and UL99 is essential for virus replication.Journal of virology · 2012Article
- Human herpesvirus 6 major immediate early promoter has strong activity in T cells and is useful for heterologous gene expression.Virology journal · 2011Article
- A systematic approach for the identification of novel, serologically reactive recombinant Varicella-Zoster Virus (VZV) antigens.Virology journal · 2010Article
- Characterization of the varicella-zoster virus ORF50 gene, which encodes glycoprotein M.Journal of virology · 2010Article
- The varicella-zoster virus genome.Current topics in microbiology and immunology · 2010Review
- Effects of simultaneous deletion of pUL11 and glycoprotein M on virion maturation of herpes simplex virus type 1.Journal of virology · 2009Article
- Varicella-zoster virus open reading frame 66 protein kinase is required for efficient viral growth in primary human corneal stromal fibroblast cells.Journal of virology · 2008Article
- Varicella-zoster virus glycoprotein M homolog is glycosylated, is expressed on the viral envelope, and functions in virus cell-to-cell spread.Journal of virology · 2008Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ORF49 gene product (ORF49p) of the varicella-zoster virus (VZV) is likely a myristylated tegument protein, and its homologs are conserved across the herpesvirus subfamilies. The UL11 gene of herpes simplex virus type 1 and of pseudorabies virus and the UL99 gene of human cytomegalovirus are the homologs of ORF49 and have been well characterized by using mutant viruses; however, little research on the VZV ORF49 gene has been reported. Here we report on VZV ORF49p expression, subcellular localization, and effect on viral spread in vitro. ORF49p was expressed during the late phase of infection and located in the juxtanuclear region of the cytoplasm, where it colocalized mainly with the trans-Golgi network-associated protein. ORF49p was incorporated into virions and showed a molecular mass of 13 kDa in VZV-infected cells and virions. To elucidate the role of the ORF49 gene, we constructed a mutant virus that lacked a functional ORF49. No differences in plaque size or cell-cell spread were observed in human embryonic fibroblast cells, MRC-5 cells, infected with the wild-type or the mutant virus. However, the mutant virus showed diminished cell-cell infection in a human malignant melanoma cell line, MeWo cells. Therefore, VZV ORF49p is important for virus growth in MeWo cells, but not in MRC-5 cells. VZV may use different mechanisms for virus growth in MeWo and MRC-5 cells. If so, understanding the role of ORF49p should help elucidate how VZV accomplishes cell-cell infections in different cell types.
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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.