Oseltamivir Is Effective against 1918 Influenza Virus Infection of Macaques but Vulnerable to Escape.
Identifieur interne : 000082 ( PubMed/Curation ); précédent : 000081; suivant : 000083Oseltamivir Is Effective against 1918 Influenza Virus Infection of Macaques but Vulnerable to Escape.
Auteurs : Friederike Feldmann [Canada] ; Darwyn Kobasa [Canada] ; Carissa Embury-Hyatt [Canada] ; Allen Grolla [Canada] ; Tracy Taylor [Canada] ; Maki Kiso [Japon] ; Satoshi Kakugawa [Japon] ; Jason Gren [Canada] ; Steven M. Jones [Canada] ; Yoshihiro Kawaoka [États-Unis] ; Heinz Feldmann [États-Unis]Source :
- mBio [ 2150-7511 ] ; 2019.
Descripteurs français
- KwdFr :
- MESH :
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- traitement médicamenteux : Infections à Orthomyxoviridae.
- usage thérapeutique : Oséltamivir.
- virologie : Infections à Orthomyxoviridae.
- Animaux, Macaca, Sous-type H1N1 du virus de la grippe A.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Oseltamivir.
- drug effects : Influenza A Virus, H1N1 Subtype.
- drug therapy : Orthomyxoviridae Infections.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- virology : Orthomyxoviridae Infections.
- Animals, Macaca.
Abstract
The 1918 influenza virus, subtype H1N1, was the causative agent of the most devastating pandemic in the history of infectious diseases. In vitro studies have confirmed that extreme virulence is an inherent property of this virus. Here, we utilized the macaque model for evaluating the efficacy of oseltamivir phosphate against the fully reconstructed 1918 influenza virus in a highly susceptible and relevant disease model. Our findings demonstrate that oseltamivir phosphate is effective in preventing severe disease in macaques but vulnerable to virus escape through emergence of resistant mutants, especially if given in a treatment regimen. Nevertheless, we conclude that oseltamivir would be highly beneficial to reduce the morbidity and mortality rates caused by a highly pathogenic influenza virus although it would be predicted that resistance would likely emerge with sustained use of the drug.IMPORTANCE Oseltamivir phosphate is used as a first line of defense in the event of an influenza pandemic prior to vaccine administration. Treatment failure through selection and replication of drug-resistant viruses is a known complication in the field and was also demonstrated in our study with spread of resistant 1918 influenza virus in multiple respiratory tissues. This emphasizes the importance of early treatment and the possibility that noncompliance may exacerbate treatment effectiveness. It also demonstrates the importance of implementing combination therapy and vaccination strategies as soon as possible in a pandemic situation.
DOI: 10.1128/mBio.02059-19
PubMed: 31641086
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<front><div type="abstract" xml:lang="en">The 1918 influenza virus, subtype H1N1, was the causative agent of the most devastating pandemic in the history of infectious diseases. <i>In vitro</i>
studies have confirmed that extreme virulence is an inherent property of this virus. Here, we utilized the macaque model for evaluating the efficacy of oseltamivir phosphate against the fully reconstructed 1918 influenza virus in a highly susceptible and relevant disease model. Our findings demonstrate that oseltamivir phosphate is effective in preventing severe disease in macaques but vulnerable to virus escape through emergence of resistant mutants, especially if given in a treatment regimen. Nevertheless, we conclude that oseltamivir would be highly beneficial to reduce the morbidity and mortality rates caused by a highly pathogenic influenza virus although it would be predicted that resistance would likely emerge with sustained use of the drug.<b>IMPORTANCE</b>
Oseltamivir phosphate is used as a first line of defense in the event of an influenza pandemic prior to vaccine administration. Treatment failure through selection and replication of drug-resistant viruses is a known complication in the field and was also demonstrated in our study with spread of resistant 1918 influenza virus in multiple respiratory tissues. This emphasizes the importance of early treatment and the possibility that noncompliance may exacerbate treatment effectiveness. It also demonstrates the importance of implementing combination therapy and vaccination strategies as soon as possible in a pandemic situation.</div>
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<Abstract><AbstractText>The 1918 influenza virus, subtype H1N1, was the causative agent of the most devastating pandemic in the history of infectious diseases. <i>In vitro</i>
studies have confirmed that extreme virulence is an inherent property of this virus. Here, we utilized the macaque model for evaluating the efficacy of oseltamivir phosphate against the fully reconstructed 1918 influenza virus in a highly susceptible and relevant disease model. Our findings demonstrate that oseltamivir phosphate is effective in preventing severe disease in macaques but vulnerable to virus escape through emergence of resistant mutants, especially if given in a treatment regimen. Nevertheless, we conclude that oseltamivir would be highly beneficial to reduce the morbidity and mortality rates caused by a highly pathogenic influenza virus although it would be predicted that resistance would likely emerge with sustained use of the drug.<b>IMPORTANCE</b>
Oseltamivir phosphate is used as a first line of defense in the event of an influenza pandemic prior to vaccine administration. Treatment failure through selection and replication of drug-resistant viruses is a known complication in the field and was also demonstrated in our study with spread of resistant 1918 influenza virus in multiple respiratory tissues. This emphasizes the importance of early treatment and the possibility that noncompliance may exacerbate treatment effectiveness. It also demonstrates the importance of implementing combination therapy and vaccination strategies as soon as possible in a pandemic situation.</AbstractText>
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<AffiliationInfo><Affiliation>School of Public Health, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.</Affiliation>
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<ForeName>Yoshihiro</ForeName>
<Initials>Y</Initials>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama, Japan.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Feldmann</LastName>
<ForeName>Heinz</ForeName>
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<AffiliationInfo><Affiliation>National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada kawaokay@svm.vetmed.wisc.edu feldmannh@niaid.nih.gov.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada.</Affiliation>
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