Comparison of the protection of ferrets against pandemic 2009 influenza A virus (H1N1) by 244 DI influenza virus and oseltamivir
► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2μg intranasal dose of DI RNA delivered as DI virus. ► Or we treated ferrets with 10 oral doses of Tamiflu totalling 25mg over 5days. ► Pandemic A/California/04/09 amplified the DI RNA by...
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| Published in | Antiviral research Vol. 96; no. 3; pp. 376 - 385 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Kidlington
Elsevier B.V
01.12.2012
Elsevier |
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| Online Access | Get full text |
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| Abstract | ► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2μg intranasal dose of DI RNA delivered as DI virus. ► Or we treated ferrets with 10 oral doses of Tamiflu totalling 25mg over 5days. ► Pandemic A/California/04/09 amplified the DI RNA by >25,000-fold. ► DI virus was more effective than Tamiflu in combatting pandemic A/California/04/09.
The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. |
|---|---|
| AbstractList | ► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2 μg intranasal dose of DI RNA delivered as DI virus. ► Or we treated ferrets with 10 oral doses of Tamiflu totalling 25 mg over 5 days. ► Pandemic A/California/04/09 amplified the DI RNA by >25,000-fold. ► DI virus was more effective than Tamiflu in combatting pandemic A/California/04/09.
The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2 μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25 mg/kg body weight of oseltamivir given as 10 oral doses over 5 days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2 mu g intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2 μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5 days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2 μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5 days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09.The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2 μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5 days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. ► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2μg intranasal dose of DI RNA delivered as DI virus. ► Or we treated ferrets with 10 oral doses of Tamiflu totalling 25mg over 5days. ► Pandemic A/California/04/09 amplified the DI RNA by >25,000-fold. ► DI virus was more effective than Tamiflu in combatting pandemic A/California/04/09. The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase. These have to be deployed close to the time of infection and antiviral resistance to the more widely used oseltamivir has arisen relatively rapidly. Defective interfering (DI) influenza virus is a natural antiviral that works in a different way to oseltamivir and zanamivir, and a cloned version (segment 1 244 DI RNA in a cloned A/PR/8/34 virus; 244/PR8) has proved effective in preclinical studies in mice. The active principle is the DI RNA, and this is thought to interact with all influenza A viruses by inhibiting RNA virus synthesis and packaging of the cognate virion RNA into nascent DI virus particles. We have compared the ability of DI virus and oseltamivir to protect ferrets from intranasal 2009 pandemic influenza virus A/California/04/09 (A/Cal, H1N1). Ferrets were treated with a single 2μg intranasal dose of 244 DI RNA delivered as 244/PR8 virus, or a total of 25mg/kg body weight of oseltamivir given as 10 oral doses over 5days. Both DI virus and oseltamivir reduced day 2 infectivity and the influx of cells into nasal fluids, and permitted the development of adaptive immunity. However DI virus, but not oseltamivir, significantly reduced weight loss, facilitated better weight gain, reduced respiratory disease, and reduced infectivity on days 4 and 6. 244 DI RNA was amplified by A/Cal by >25,000-fold, consistent with the amelioration of clinical disease. Treatment with DI virus did not delay clearance or cause persistence of infectious virus or DI RNA. Thus in this system DI virus was overall more effective than oseltamivir in combatting pandemic A/California/04/09. |
| Author | Cheung, Linda Dimmock, Nigel J. Dove, Brian K. Meng, Bo Taylor, Irene Scott, Paul D. Marriott, Anthony C. Easton, Andrew J. Hallis, Bassam Carroll, Miles W. |
| AuthorAffiliation | b Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK a School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK |
| AuthorAffiliation_xml | – name: b Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK – name: a School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK |
| Author_xml | – sequence: 1 givenname: Nigel J. surname: Dimmock fullname: Dimmock, Nigel J. email: n.j.dimmock@warwick.ac.uk organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK – sequence: 2 givenname: Brian K. surname: Dove fullname: Dove, Brian K. organization: Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK – sequence: 3 givenname: Bo surname: Meng fullname: Meng, Bo organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK – sequence: 4 givenname: Paul D. surname: Scott fullname: Scott, Paul D. organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK – sequence: 5 givenname: Irene surname: Taylor fullname: Taylor, Irene organization: Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK – sequence: 6 givenname: Linda surname: Cheung fullname: Cheung, Linda organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK – sequence: 7 givenname: Bassam surname: Hallis fullname: Hallis, Bassam organization: Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK – sequence: 8 givenname: Anthony C. surname: Marriott fullname: Marriott, Anthony C. organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK – sequence: 9 givenname: Miles W. surname: Carroll fullname: Carroll, Miles W. organization: Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK – sequence: 10 givenname: Andrew J. surname: Easton fullname: Easton, Andrew J. organization: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK |
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| Keywords | Oseltamivir Influenza virus Protection Defective interfering virus Ferret Fissipedia Carnivora Neuraminidase inhibitor Enzyme Enzyme inhibitor Glycosylases Virus Vertebrata Mammalia Exo-α-sialidase Glycosidases Hydrolases Antiviral Comparative study |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 These authors contributed equally to this study. Present address: Health Protection Agency, Porton Down, Salisbury SP4 0JG, UK. |
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| Snippet | ► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2μg intranasal dose of DI RNA delivered as DI... The main antivirals employed to combat seasonal and pandemic influenza are oseltamivir and zanamivir which act by inhibiting the virus-encoded neuraminidase.... ► We compared the ability of DI RNA and Tamiflu to protect ferrets from influenza. ► We treated ferrets with one 2 μg intranasal dose of DI RNA delivered as DI... |
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| SubjectTerms | Animals Antibiotics. Antiinfectious agents. Antiparasitic agents Antiviral agents Antiviral Agents - pharmacology Biological and medical sciences Body weight Cell Line Defective interfering virus Defective Viruses - immunology Exo- alpha -sialidase Ferret Ferrets - immunology Ferrets - virology Hemagglutination Inhibition Tests Immunity Infection Infectivity Influenza Influenza A Influenza A virus Influenza A Virus, H1N1 Subtype - immunology Influenza A Virus, H1N1 Subtype - pathogenicity Influenza virus Male Medical sciences Mustela Nasal Lavage Fluid - virology Obesity Orthomyxoviridae Infections - drug therapy Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - prevention & control Oseltamivir Oseltamivir - pharmacology Packaging pandemics Particulates Pharmacology. Drug treatments Protection Respiratory diseases RNA viruses RNA, Viral - immunology Seasonal variations Sulfur dioxide Transfection Virions Viruses Weight Loss Zanamivir |
| Title | Comparison of the protection of ferrets against pandemic 2009 influenza A virus (H1N1) by 244 DI influenza virus and oseltamivir |
| URI | https://dx.doi.org/10.1016/j.antiviral.2012.09.017 https://www.ncbi.nlm.nih.gov/pubmed/23041142 https://www.proquest.com/docview/1221850101 https://www.proquest.com/docview/1257738392 https://pubmed.ncbi.nlm.nih.gov/PMC3526778 |
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