ArticleCell2020
SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses.
Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 389 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
389 citing papers in PubMed, 1 synthesis or guideline pooled it, 623 citations in OpenAlex.
- An integrative meta-analysis of SARS-CoV-2 RNA-protein interactomes identifies conserved host factors shared with other RNA viruses.Briefings in functional genomics · 2026Pooled it
- Loss of cellular RNA homeostasis contributes to MDA5 activation during virus infection.Nature immunology · 2026Article
- Exploring the role of differential splicing of Pekin ducks resistant to DHAV-3 based on full-length transcriptome.Poultry science · 2026Article
- Article
- Mind the gap between RNA and protein levels: A general phenomenon with implications for virology.PLoS pathogens · 2026Article
- SARS-CoV-2 ORF3a suppresses host antiviral interferon responses by promoting STUB1-mediated PTEN proteasomal degradation.Journal of virology · 2026Article
- Mechanism and key RNA determinants of SARS-CoV-2 Nsp1-induced endonucleolytic cleavage of mRNA.bioRxiv : the preprint server for biology · 2026Article
- Reprogramming innate immunity through viral interference: A double-edged strategy for enhancing and containing gene therapies.Molecular therapy. Nucleic acids · 2026Review
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- Structure and sequence characteristics of 5'-stem-loop 1 modulate the escape from nsp1-mediated repression in SARS-CoV-2 variants.Nucleic acids research · 2026Article
- Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer.bioRxiv : the preprint server for biology · 2026Article
- Transcriptional and Alternative Splicing Regulation of Autophagy and Vesicle Transport Pathways in Large Yellow Croaker Cells During Megalocytivirus Infection.Animals : an open access journal from MDPI · 2026Article
- SARS-CoV-2 and MERS-CoV disrupt host protein synthesis via nsp1 with differential effects on the integrated stress response.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Proteoform medicine: characterizing and targeting protein forms in human disease.Nature reviews. Genetics · 2026Review
- Ribosome Molecular Aging Shapes Translation Dynamics.bioRxiv : the preprint server for biology · 2026Article
- Impact of nutrition on long COVID.Sports medicine and health science · 2026Review
- Article
- YL1004 is a SARS-CoV-2 papain-like protease inhibitor with immunomodulatory and antiviral activity in mice.Nature communications · 2026Article
- A bacterial translation activator with an intrinsically disordered RNA-binding region.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Strategic variations in sarbecovirus and merbecovirus Nsp1 linker regions for translation inhibition.Nucleic acids research · 2026Article
329 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 2 countries.
Funding
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a recently identified coronavirus that causes the respiratory disease known as coronavirus disease 2019 (COVID-19). Despite the urgent need, we still do not fully understand the molecular basis of SARS-CoV-2 pathogenesis. Here, we comprehensively define the interactions between SARS-CoV-2 proteins and human RNAs. NSP16 binds to the mRNA recognition domains of the U1 and U2 splicing RNAs and acts to suppress global mRNA splicing upon SARS-CoV-2 infection. NSP1 binds to 18S ribosomal RNA in the mRNA entry channel of the ribosome and leads to global inhibition of mRNA translation upon infection. Finally, NSP8 and NSP9 bind to the 7SL RNA in the signal recognition particle and interfere with protein trafficking to the cell membrane upon infection. Disruption of each of these essential cellular functions acts to suppress the interferon response to viral infection. Our results uncover a multipronged strategy utilized by SARS-CoV-2 to antagonize essential cellular processes to suppress host defenses.
Indexed as
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What Socratic holds
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.