Cited by 125Cystic Fibrosis Research Advancesinterferon and immune responsesImmunodeficiency and Autoimmune Disorders

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Impaired Innate Host Defense Causes Susceptibility to Respiratory Virus Infections in Cystic Fibrosis

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Zheng, Shuo, De, Bishnu P, Choudhary, Suresh, Comhair, Suzy A.A, Goggans, Tannishia, Slee, Roger, Williams, Bryan R.G, Pilewski, Joseph, Haque, S.Jaharul, Erzurum, Serpil C·2003·Immunity

DOI 10.1016/s1074-7613(03)00114-6

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Abstract

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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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: Zheng, Shuo
Choudhary, Suresh
Comhair, Suzy A.A
Williams, Bryan R.G
Pilewski, Joseph
Haque, S.Jaharul
Erzurum, Serpil C
Venue: Immunity
Publisher: Elsevier BV
Published: 2003-05
Volume: 18
Issue: 5
Pages: 619-630
ISSN: 1074-7613 (ISSN-L)
DOI: 10.1016/s1074-7613(03)00114-6
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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Impaired Innate Host Defense Causes Susceptibility to Respiratory Virus Infections in Cystic Fibrosis

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