ArticlePLoS pathogens2021
SARS-CoV-2 suppresses IFNβ production mediated by NSP1, 5, 6, 15, ORF6 and ORF7b but does not suppress the effects of added interferon.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 140 citations in OpenAlex.
- Selective decay of interferon mRNAs controls antiviral immunity and innate memory.Molecular cell · 2026Article
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- Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during Viral Infection.Journal of microbiology and biotechnology · 2026Review
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- Inhibiting the interaction between the mitochondrial receptor Tom70 and SARS CoV 2 Orf9b with small molecules.bioRxiv : the preprint server for biology · 2026Article
- Entry, replication and innate immunity evasion of BANAL-236, a SARS-CoV-2-related bat virus, in Rhinolophus and human cells.PLoS pathogens · 2026Article
- Review
- Interactions of SARS-CoV-2, influenza and respiratory syncytial virus influence epidemic timing and risk.Communications medicine · 2026Article
- SARS-CoV-2 Nsp15 facilitates immune evasion and viral replication by limiting multiple host innate immune pathways, including cGAS-STING.The Journal of general virology · 2026Article
- Heterogeneity of Airborne Virus Transmission in the Built Environment: A Narrative Review.Pathogens & immunity · 2026Review
- Innate immune activation profiles are associated with polarization of the T cell response to recombinant arenaviral vectors.Frontiers in systems biology · 2026Article
- Porcine Deltacoronavirus Nsp13 Suppresses the Assembly of the MAVS-TBK1-IRF3 Complex and IRF9 Nuclear Translocation.Transboundary and emerging diseases · 2026Article
- Article
- SARS-CoV-2-derived RNA replicons as safe and effective vaccines.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- The role of SARS-CoV-2 main protease in innate immune regulation: From molecular mechanisms to therapeutic implications.Acta pharmaceutica Sinica. B · 2025Review
- NSP6 regulates calcium overload-induced autophagic cell death and is regulated by KLHL22-mediated ubiquitination.Journal of advanced research · 2025Article
- Article
- The P132H mutation of SARS-CoV-2 NSP5 relieves its inhibition on interferon-β activation via blocking MAVS degradation.Cellular and molecular life sciences : CMLS · 2025Article
- SARS-CoV-2 encoded ORF3a interacts with YY1 to promote latent HCMV reactivation.PLoS pathogens · 2025Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I Interferons (IFN-Is) are a family of cytokines which play a major role in inhibiting viral infection. Resultantly, many viruses have evolved mechanisms in which to evade the IFN-I response. Here we tested the impact of expression of 27 different SARS-CoV-2 genes in relation to their effect on IFN production and activity using three independent experimental methods. We identified six gene products; NSP6, ORF6, ORF7b, NSP1, NSP5 and NSP15, which strongly (>10-fold) blocked MAVS-induced (but not TRIF-induced) IFNβ production. Expression of the first three of these SARS-CoV-2 genes specifically blocked MAVS-induced IFNβ-promoter activity, whereas all six genes induced a collapse in IFNβ mRNA levels, corresponding with suppressed IFNβ protein secretion. Five of these six genes furthermore suppressed MAVS-induced activation of IFNλs, however with no effect on IFNα or IFNγ production. In sharp contrast, SARS-CoV-2 infected cells remained extremely sensitive to anti-viral activity exerted by added IFN-Is. None of the SARS-CoV-2 genes were able to block IFN-I signaling, as demonstrated by robust activation of Interferon Stimulated Genes (ISGs) by added interferon. This, despite the reduced levels of STAT1 and phospho-STAT1, was likely caused by broad translation inhibition mediated by NSP1. Finally, we found that a truncated ORF7b variant that has arisen from a mutant SARS-CoV-2 strain harboring a 382-nucleotide deletion associating with mild disease (Δ382 strain identified in Singapore & Taiwan in 2020) lost its ability to suppress type I and type III IFN production. In summary, our findings support a multi-gene process in which SARS-CoV-2 blocks IFN-production, with ORF7b as a major player, presumably facilitating evasion of host detection during early infection. However, SARS-CoV-2 fails to suppress IFN-I signaling thus providing an opportunity to exploit IFN-Is as potential therapeutic antiviral drugs.
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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.