ArticleJournal of virology2020
Conserved Herpesvirus Kinase ORF36 Activates B2 Retrotransposons during Murine Gammaherpesvirus Infection.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 16 citations in OpenAlex.
- Promoter-associated RNA polymerase III shapes RNA polymerase II-dependent inflammatory gene expression during viral infection.bioRxiv : the preprint server for biology · 2026Article
- Essentiality and dynamic expression of the human tRNA pool during viral infection.Molecular systems biology · 2026Article
- RNA polymerase III transcription-associated polyadenylation promotes the accumulation of noncoding retrotransposons during infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- "Transfer" of power: The intersection of DNA virus infection and tRNA biology.Seminars in cell & developmental biology · 2023Review
- Article
- Mechanism of herpesvirus protein kinase UL13 in immune escape and viral replication.Frontiers in immunology · 2022Review
- DDX17 is an essential mediator of sterile NLRC4 inflammasome activation by retrotransposon RNAs.Science immunology · 2021Article
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- Lytic Infection with Murine Gammaherpesvirus 68 Activates Host and Viral RNA Polymerase III Promoters and Enhances Noncoding RNA Expression.Journal of virology · 2021Article
- Article
- Modification of Nuclear Compartments and the 3D Genome in the Course of a Viral Infection.Acta naturaeArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Short interspersed nuclear elements (SINEs) are RNA polymerase III (RNAPIII)-transcribed, retrotransposable noncoding RNA (ncRNA) elements ubiquitously spread throughout mammalian genomes. While normally silenced in healthy somatic tissue, SINEs can be induced during infection with DNA viruses, including the model murine gammaherpesvirus 68 (MHV68). Here, we explored the mechanisms underlying MHV68 activation of SINE ncRNAs. We demonstrate that lytic MHV68 infection of B cells, macrophages, and fibroblasts leads to robust activation of the B2 family of SINEs in a cell-autonomous manner. B2 ncRNA induction requires neither host innate immune signaling factors nor involvement of the RNAPIII master regulator Maf1. However, we identified MHV68 ORF36, the conserved herpesviral kinase, as playing a key role in B2 induction during lytic infection. SINE activation is linked to ORF36 kinase activity and can also be induced by inhibition of histone deacetylases 1 and 2 (HCAC 1/2), which is one of the known ORF36 functions. Collectively, our data suggest that ORF36-mediated changes in chromatin modification contribute to B2 activation during MHV68 infection and that this activity is conserved in other herpesviral protein kinase homologs.
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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 Socratic graph.