The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated Strain
Open accessAbstract
The severe acute respiratory syndrome (SARS) epidemic was caused by the spread of a previously unrecognized infectious agent, the SARS-associated coronavirus (SARS-CoV). Here we show that SARS-CoV could inhibit both virus- and interferon (IFN)-dependent signaling, two key steps of the antiviral response. We mapped a strong inhibitory activity to SARS-CoV nonstructural protein 1 (nsp1) and show that expression of nsp1 significantly inhibited the activation of all three virus-dependent signaling pathways. We show that expression of nsp1 significantly inhibited IFN-dependent signaling by decreasing the phosphorylation levels of STAT1 while having little effect on those of STAT2, JAK1, and TYK2. We engineered an attenuated mutant of nsp1 in SARS-CoV through reverse genetics, and the resulting mutant virus was viable and replicated as efficiently as wild-type virus in cells with a defective IFN response. However, mutant virus replication was strongly attenuated in cells with an intact IFN response. Thus, nsp1 is likely a virulence factor that contributes to pathogenicity by favoring SARS-CoV replication.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Identification of a novel coronavirus in patients with severe acute respiratory syndrome
Drosten, C., Günther, S., Preiser, W., van der Werf, S., Brodt, H.-R., Becker, S., Rabenau, H., Panning, M., Kolesnikova, L., Fouchier, R. A. M., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa030747 · Cited by 4,574
Innate immune recognition of viral infection
Kawai, T., & Akira, S. (2006) · Nature Immunology · doi:10.1038/ni1303 · Cited by 1,899
Wathelet, M. G., Lin, C. H., Parekh, B. S., Ronco, L. V., Howley, P. M., & Maniatis, T. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80051-9 · Cited by 730
Self-citationThe virus battles: IFN induction of the antiviral state and mechanisms of viral evasion
Levy, D. (2001) · Cytokine & Growth Factor Reviews · doi:10.1016/s1359-6101(00)00027-7 · Cited by 428
Cited by
SARS and MERS: recent insights into emerging coronaviruses
de Wit, E., van Doremalen, N., Falzarano, D., & Munster, V. J. (2016) · Nature Reviews Microbiology · doi:10.1038/nrmicro.2016.81 · Cited by 3,510
Channappanavar, R., & Perlman, S. (2017) · Seminars in Immunopathology · doi:10.1007/s00281-017-0629-x · Cited by 2,524
Coronaviruses post-SARS: update on replication and pathogenesis
Perlman, S., & Netland, J. (2009) · Nature Reviews Microbiology · doi:10.1038/nrmicro2147 · Cited by 1,764
Immunology of COVID-19: Current State of the Science
Vabret, N., Britton, G. J., Gruber, C., Hegde, S., Kim, J., Kuksin, M., Levantovsky, R., Malle, L., Moreira, A., Park, M. D., et al. (2020) · Immunity · doi:10.1016/j.immuni.2020.05.002 · Cited by 1,623
Type I and Type III Interferons – Induction, Signaling, Evasion, and Application to Combat COVID-19
Park, A., & Iwasaki, A. (2020) · Cell Host & Microbe · doi:10.1016/j.chom.2020.05.008 · Cited by 909
Metadata
- Authors
- Wathelet, M. G., Orr, M., Frieman, M. B., & Baric, R. S.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2007-11
- Volume
- 81
- Issue
- 21
- Pages
- 11620-11633
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- OpenAlex
- W2068070201
- Cited by
- 345
- References
- 4
- FWCI
- 8.23
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated Strain. https://app.cochat.ai/papers/10.1128/jvi.00702-07
- The paper
- Wathelet, M. G., Orr, M., Frieman, M. B., & Baric, R. S. (2007). Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated Strain. Journal of Virology. https://doi.org/10.1128/jvi.00702-07
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
