Impaired Innate Host Defense Causes Susceptibility to Respiratory Virus Infections in Cystic Fibrosis
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...
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| Published in: | Immunity (Cambridge, Mass.) Vol. 18; no. 5; pp. 619 - 630 |
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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 IFNγ. 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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| AbstractList | 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 IFN gamma . 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. 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. 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 IFNγ. 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. |
| Author | Williams, Bryan R.G Pilewski, Joseph Erzurum, Serpil C De, Bishnu P Slee, Roger Haque, S.Jaharul Comhair, Suzy A.A Zheng, Shuo Goggans, Tannishia Choudhary, Suresh |
| Author_xml | – sequence: 1 givenname: Shuo surname: Zheng fullname: Zheng, Shuo organization: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 2 givenname: Bishnu P surname: De fullname: De, Bishnu P organization: Department of Virology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 3 givenname: Suresh surname: Choudhary fullname: Choudhary, Suresh organization: Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 4 givenname: Suzy A.A surname: Comhair fullname: Comhair, Suzy A.A organization: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 5 givenname: Tannishia surname: Goggans fullname: Goggans, Tannishia organization: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 6 givenname: Roger surname: Slee fullname: Slee, Roger organization: Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 7 givenname: Bryan R.G surname: Williams fullname: Williams, Bryan R.G organization: Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 8 givenname: Joseph surname: Pilewski fullname: Pilewski, Joseph organization: Departments of Medicine, Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA 15261 USA – sequence: 9 givenname: S.Jaharul surname: Haque fullname: Haque, S.Jaharul organization: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA – sequence: 10 givenname: Serpil C surname: Erzurum fullname: Erzurum, Serpil C email: erzurus@ccf.org organization: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA |
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| Snippet | Viral infection is the primary cause of respiratory morbidity in cystic fibrosis (CF) infants. Here, we identify that host factors allow increased virus... |
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| SubjectTerms | Antiviral Agents - pharmacology Cystic fibrosis Cystic Fibrosis - complications Cystic Fibrosis - immunology Cystic Fibrosis - virology Disease Susceptibility - immunology Humans Immunity, Innate - immunology In Vitro Techniques Infections Interferon Interferons - pharmacology Kinases Nitric Oxide Donors - metabolism Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Parainfluenza Virus 3, Human Respirovirus Infections - complications Respirovirus Infections - drug therapy Respirovirus Infections - immunology Transcription Factors - metabolism Viral infections |
| Title | Impaired Innate Host Defense Causes Susceptibility to Respiratory Virus Infections in Cystic Fibrosis |
| URI | https://dx.doi.org/10.1016/S1074-7613(03)00114-6 https://www.ncbi.nlm.nih.gov/pubmed/12753739 https://www.proquest.com/docview/1504203914 https://search.proquest.com/docview/18806104 https://search.proquest.com/docview/73317292 |
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