ArticleJournal of virology2019
C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi's Sarcoma-Associated Herpesvirus.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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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.
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Who cites it
37 citing papers in PubMed, 44 citations in OpenAlex.
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- Porcine reproductive and respiratory syndrome virus antagonizes the host restriction factor SHFL to sustain viral programmed ribosomal frameshifting and replication.Journal of virology · 2026Article
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- The anti-viral protein Shiftless blocks p-body formation during KSHV infection.The Journal of general virology · 2026Article
- Phosphorylation of shiftless is important for inhibiting the programmed -1 ribosomal frameshift.Science advances · 2025Article
- Virally encoded interleukin-6 (vIL-6) coordinates with human IL-6 to modulate cytokine expression during KSHV infection.bioRxiv : the preprint server for biology · 2025Article
- Stem loop binding protein promotes SARS-CoV-2 replication via -1 programmed ribosomal frameshifting.Signal transduction and targeted therapy · 2025Article
- Antiviral potential of diosmin against influenza A virus.Scientific reports · 2025Article
- Genetic variations of thePeerJ · 2025Article
- Interferon induced circRNAs escape herpesvirus host shutoff and suppress lytic infection.EMBO reports · 2024Article
- Mechanisms and consequences of mRNA destabilization during viral infections.Virology journal · 2024Review
- Mouse Liver-Expressed Shiftless Is an Evolutionarily Conserved Antiviral Effector Restricting Human and Murine Hepaciviruses.Microbiology spectrum · 2023Article
- The cellular and KSHV A-to-I RNA editome in primary effusion lymphoma and its role in the viral lifecycle.Nature communications · 2023Article
- Review
- Functional features of a novel interferon-stimulated gene SHFL: a comprehensive review.Frontiers in microbiology · 2023Review
- Association of genetic polymorphisms in theFrontiers in cellular and infection microbiology · 2023Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- Restriction of Flaviviruses by an Interferon-Stimulated Gene SHFL/C19orf66.International journal of molecular sciences · 2022Review
- The Role of Viral RNA Degrading Factors in Shutoff of Host Gene Expression.Annual review of virology · 2022Review
- Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One striking characteristic of certain herpesviruses is their ability to induce rapid and widespread RNA decay in order to gain access to host resources. This phenotype is induced by viral endoribonucleases, including SOX in Kaposi's sarcoma-associated herpesvirus (KSHV), muSOX in murine gammaherpesvirus 68 (MHV68), BGLF5 in Epstein-Barr virus (EBV), and vhs in herpes simplex virus 1 (HSV-1). Here, we performed comparative transcriptome sequencing (RNA-seq) upon expression of these herpesviral endonucleases in order to characterize their effect on the host transcriptome. Consistent with previous reports, we found that approximately two-thirds of transcripts were downregulated in cells expressing any of these viral endonucleases. Among the transcripts spared from degradation, we uncovered a cluster of transcripts that systematically escaped degradation from all tested endonucleases. Among these escapees, we identified C19ORF66 and reveal that this transcript is protected from degradation by its 3' untranslated region (UTR). We then show that C19ORF66 is a potent KSHV restriction factor by impeding early viral gene expression, suggesting that its ability to escape viral cleavage may be an important component of the host response to viral infection. Collectively, our comparative approach is a powerful tool to pinpoint key regulators of the viral-host interplay and led us to uncover a novel KSHV regulator.
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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 OpenQuestion graph.