The DOI matches its Crossref record; 81 of the 82 references it cites were found in a registry or an index.
Impaired Innate Host Defense Causes Susceptibility to Respiratory Virus Infections in Cystic Fibrosis
Open accessAbstract
Viral infection is the primary cause of respiratory morbidity in cystic fibrosis (CF) infants. Here, we identify that host factors allow increased virus replication and cytokine production, providing a mechanism for understanding the severity of virus disease in CF. Increased virus is due to lack of nitric oxide synthase 2 (NOS2) and 2', 5' oligoadenylate synthetase (OAS) 1 induction in response to virus or IFNgamma. This can be attributed to impairment of activation of signal transducer and activator of transcription (STAT)1, a fundamental component to antiviral defense. NO donor or NOS2 overexpression provides protection from virus infection in CF, suggesting that NO is sufficient for antiviral host defense in the human airway and is one strategy for antiviral therapy in CF children.
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“Airway mucin production is induced by many respiratory viruses, including rhinovirus and influenza virus (278, 336).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [336]
Citations
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Metadata
- Authors
- Zheng, S., De, B. P., Choudhary, S., Comhair, S. A. A., Goggans, T., Slee, R., Williams, B. R. G., Pilewski, J., Haque, S. J., & Erzurum, S. C.
- Affiliations
- Cleveland Clinic (US)
- University of Pittsburgh (US)
- Corresponding author
- Erzurum, Serpil C
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2003-05
- Volume
- 18
- Issue
- 5
- Pages
- 619-630
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2025877008
- Cited by
- 125
- References
- 82
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 5 · 2021: 7 · 2020: 9 · 2019: 5 · 2018: 1 · 2017: 4 · 2016: 7 · 2015: 5 · 2014: 8 · 2013: 9 · 2012: 11
- FWCI
- 5.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 3730 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cystic Fibrosis Foundation
- National Institutes of Health (P50 DK56490)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cystic Fibrosis Research Advances
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Keywords
- cystic fibrosis, respiratory viral infections, antiviral innate immunity, nitric oxide synthase 2, 2',5'-oligoadenylate synthetase, STAT1 signaling, interferon-gamma, nitric oxide, cytokine production, viral replication, airway immunity, antiviral therapy
- MeSH terms
- Antiviral Agents, Cystic Fibrosis, Disease Susceptibility, Humans, Immunity, Innate, Interferons, Parainfluenza Virus 3, Human, Respirovirus Infections, Transcription Factors, Nitric Oxide Synthase, Nitric Oxide Donors, Nitric Oxide Synthase Type II, In Vitro Techniques
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