ArticleJournal of virology2013
An RNA element in human interleukin 6 confers escape from degradation by the gammaherpesvirus SOX protein.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 43 citations in OpenAlex.
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- Targeting the ROS-ferroptosis-inflammation cycle with a nanozyme-functionalized hydrogel for intervertebral disc repair.Nature communications · 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
- Distinct non-canonical translation initiation modes arise for specific host and viral mRNAs during poxvirus-induced shutoff.Nature microbiology · 2025Article
- Review
- Interferon induced circRNAs escape herpesvirus host shutoff and suppress lytic infection.EMBO reports · 2024Article
- Review
- Review
- DNA processing by the Kaposi's sarcoma-associated herpesvirus alkaline exonuclease SOX contributes to viral gene expression and infectious virion production.Nucleic acids research · 2023Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- The Role of Viral RNA Degrading Factors in Shutoff of Host Gene Expression.Annual review of virology · 2022Review
- The mProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Feline Calicivirus Proteinase-Polymerase Protein Degrades mRNAs To Inhibit Host Gene Expression.Journal of virology · 2021Article
- Feline calicivirus strain 2280 p30 antagonizes type I interferon-mediated antiviral innate immunity through directly degrading IFNAR1 mRNA.PLoS pathogens · 2020Article
- Global epigenomic analysis of KSHV-infected primary effusion lymphoma identifies functionalProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Fine-tuning a blunt tool: Regulation of viral host shutoff RNases.PLoS pathogens · 2020Article
- C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2019Article
- Site specific target binding controls RNA cleavage efficiency by the Kaposi's sarcoma-associated herpesvirus endonuclease SOX.Nucleic acids research · 2018Article
- Going against the Tide: Selective Cellular Protein Synthesis during Virally Induced Host Shutoff.Journal of virology · 2017Review
- Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Several viruses express factors to silence host gene expression via widespread mRNA degradation. This phenotype is the result of the coordinated activity of the viral endonuclease SOX and the cellular RNA degradation enzyme Xrn1 during lytic Kaposi's sarcoma-associated herpesvirus (KSHV) infection. While most cellular transcripts are highly downregulated, a subset of host mRNA escapes turnover via unknown mechanisms. One of the most prominent escapees is the interleukin 6 (IL-6) mRNA, which accumulates robustly during KSHV lytic infection and is not subjected to SOX-induced degradation. Here we reveal that the IL-6 mRNA contains a dominant, cis-acting ∼100-nucleotide element within its 3' untranslated region (UTR) that renders it directly refractory to cleavage by SOX. This element specifically interacts with a cellular protein complex both in SOX-transfected cells and in KSHV-infected B cells. Using a directed RNA pulldown approach, we identified two components of this complex to be the AU-rich element (ARE) binding proteins AUF1 and HuR. Depletion of these proteins significantly reduced the protective capacity of the IL-6 RNA element in SOX-expressing cells. These findings suggest that SOX activity may be directly counteracted by select RNA regulatory complexes and reveal a novel mechanism contributing to the robust expression of IL-6 during KSHV replication.
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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.