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Cited by 499

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Immunopathogenesis of coronavirus infections: implications for SARS

Open access
Dandekar, Ajai A., Perlman, Stanley·2005·Nature Reviews Immunology

Abstract

At the end of 2002, the first cases of severe acute respiratory syndrome (SARS) were reported, and in the following year, SARS resulted in considerable mortality and morbidity worldwide. SARS is caused by a novel species of coronavirus (SARS-CoV) and is the most severe coronavirus-mediated human disease that has been described so far. On the basis of similarities with other coronavirus infections, SARS might, in part, be immune mediated. As discussed in this Review, studies of animals that are infected with other coronaviruses indicate that excessive and sometimes dysregulated responses by macrophages and other pro-inflammatory cells might be particularly important in the pathogenesis of disease that is caused by infection with these viruses. It is hoped that lessons from such studies will help us to understand more about the pathogenesis of SARS in humans and to prevent or control outbreaks of SARS in the future.

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Metadata

Authors
Dandekar, A. A., & Perlman, S.
Venue
Nature Reviews Immunology
Published
2005-12-01
Volume
5
Issue
12
Pages
917-927
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2016029872
Cited by
499
References
6
FWCI
1.90
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Immunopathogenesis of coronavirus infections: implications for SARS. https://app.cochat.ai/papers/10.1038/nri1732
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Dandekar, A. A., & Perlman, S. (2005). Immunopathogenesis of coronavirus infections: implications for SARS. Nature Reviews Immunology. https://doi.org/10.1038/nri1732

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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.