Inhibition of influenza A virus infection by ginsenosides.
Identifieur interne : 000324 ( PubMed/Curation ); précédent : 000323; suivant : 000325Inhibition of influenza A virus infection by ginsenosides.
Auteurs : Wei Dong [République populaire de Chine] ; Amber Farooqui [République populaire de Chine] ; Alberto J. Leon [République populaire de Chine] ; David J. Kelvin [République populaire de Chine]Source :
- PloS one [ 1932-6203 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (pharmacologie), Antiviraux (usage thérapeutique), Cellules CHO, Cellules rénales canines Madin-Darby, Chiens, Cricetinae, Cricetulus, Femelle, Ginsénosides (pharmacologie), Ginsénosides (usage thérapeutique), Glycoprotéine hémagglutinine du virus influenza (métabolisme), Infections à Orthomyxoviridae (traitement médicamenteux), Liaison aux protéines, Souris, Souris de lignée BALB C, Virus de la grippe A (pathogénicité).
- MESH :
- métabolisme : Glycoprotéine hémagglutinine du virus influenza.
- pathogénicité : Virus de la grippe A.
- pharmacologie : Antiviraux, Ginsénosides.
- traitement médicamenteux : Infections à Orthomyxoviridae.
- usage thérapeutique : Antiviraux, Ginsénosides.
- Animaux, Cellules CHO, Cellules rénales canines Madin-Darby, Chiens, Cricetinae, Cricetulus, Femelle, Liaison aux protéines, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (pharmacology), Antiviral Agents (therapeutic use), CHO Cells, Cricetinae, Cricetulus, Dogs, Female, Ginsenosides (pharmacology), Ginsenosides (therapeutic use), Hemagglutinin Glycoproteins, Influenza Virus (metabolism), Influenza A virus (pathogenicity), Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Orthomyxoviridae Infections (drug therapy), Protein Binding.
- MESH :
- chemical , metabolism : Hemagglutinin Glycoproteins, Influenza Virus.
- chemical , pharmacology : Antiviral Agents, Ginsenosides.
- chemical , therapeutic use : Antiviral Agents, Ginsenosides.
- drug therapy : Orthomyxoviridae Infections.
- pathogenicity : Influenza A virus.
- Animals, CHO Cells, Cricetinae, Cricetulus, Dogs, Female, Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Protein Binding.
Abstract
Influenza viruses cause mild to severe respiratory infections in humans. Due to efficient means of transmission, the viruses infect human population on a large scale. Apart from vaccines, antiviral drugs are used to control infection; neuraminidase inhibitors are thought to be the first choice of treatment, particularly for severe cases. Rapidly evolving and emerging influenza viruses with increased frequency of viral resistance to these drugs stress the need to explore novel antiviral compounds. In this study, we investigated antiviral activity of ginseng extract and ginsenosides, the ginseng-derived triterpene and saponin compounds, against 2009 pandemic H1N1 virus in vitro and in vivo. Our data showed that treatment of mice with ginsenosides protected the animals from lethal 2009 pandemic H1N1 infection and lowered viral titers in animal lungs. Mechanistic studies revealed that ginsenosides interact with viral hemagglutinin protein and prevent the attachment of virus with α 2-3' sialic acid receptors present on host cell surfaces. The interference in the viral attachment process subsequently minimizes viral entry into the cells and decreases the severity of the viral infection. We also describe that sugar moieties present in ginsenosides are indispensible for their attachment with viral HA protein. On the basis of our observations, we can say that ginsenosides are promising candidates for the development of antiviral drugs for influenza viruses.
DOI: 10.1371/journal.pone.0171936
PubMed: 28187149
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Due to efficient means of transmission, the viruses infect human population on a large scale. Apart from vaccines, antiviral drugs are used to control infection; neuraminidase inhibitors are thought to be the first choice of treatment, particularly for severe cases. Rapidly evolving and emerging influenza viruses with increased frequency of viral resistance to these drugs stress the need to explore novel antiviral compounds. In this study, we investigated antiviral activity of ginseng extract and ginsenosides, the ginseng-derived triterpene and saponin compounds, against 2009 pandemic H1N1 virus in vitro and in vivo. Our data showed that treatment of mice with ginsenosides protected the animals from lethal 2009 pandemic H1N1 infection and lowered viral titers in animal lungs. Mechanistic studies revealed that ginsenosides interact with viral hemagglutinin protein and prevent the attachment of virus with α 2-3' sialic acid receptors present on host cell surfaces. The interference in the viral attachment process subsequently minimizes viral entry into the cells and decreases the severity of the viral infection. We also describe that sugar moieties present in ginsenosides are indispensible for their attachment with viral HA protein. On the basis of our observations, we can say that ginsenosides are promising candidates for the development of antiviral drugs for influenza viruses.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28187149</PMID><DateCompleted><Year>2017</Year><Month>08</Month><Day>09</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>08</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>2</Issue><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Inhibition of influenza A virus infection by ginsenosides.</ArticleTitle><Pagination><MedlinePgn>e0171936</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0171936</ELocationID><Abstract><AbstractText>Influenza viruses cause mild to severe respiratory infections in humans. Due to efficient means of transmission, the viruses infect human population on a large scale. Apart from vaccines, antiviral drugs are used to control infection; neuraminidase inhibitors are thought to be the first choice of treatment, particularly for severe cases. Rapidly evolving and emerging influenza viruses with increased frequency of viral resistance to these drugs stress the need to explore novel antiviral compounds. In this study, we investigated antiviral activity of ginseng extract and ginsenosides, the ginseng-derived triterpene and saponin compounds, against 2009 pandemic H1N1 virus in vitro and in vivo. Our data showed that treatment of mice with ginsenosides protected the animals from lethal 2009 pandemic H1N1 infection and lowered viral titers in animal lungs. Mechanistic studies revealed that ginsenosides interact with viral hemagglutinin protein and prevent the attachment of virus with α 2-3' sialic acid receptors present on host cell surfaces. The interference in the viral attachment process subsequently minimizes viral entry into the cells and decreases the severity of the viral infection. We also describe that sugar moieties present in ginsenosides are indispensible for their attachment with viral HA protein. On the basis of our observations, we can say that ginsenosides are promising candidates for the development of antiviral drugs for influenza viruses.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Division of Immunology, International Institute of Infection and Immunity, University Health Network & Shantou University Medical College, Shantou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Farooqui</LastName><ForeName>Amber</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Immunology, International Institute of Infection and Immunity, University Health Network & Shantou University Medical College, Shantou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leon</LastName><ForeName>Alberto J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>Division of Immunology, International Institute of Infection and Immunity, University Health Network & Shantou University Medical College, Shantou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kelvin</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Division of Immunology, International Institute of Infection and Immunity, University Health Network & Shantou University Medical College, Shantou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Medical Science, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Deptartment of Immunology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036145">Ginsenosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019267">Hemagglutinin Glycoproteins, Influenza Virus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016466" MajorTopicYN="N">CHO Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006224" MajorTopicYN="N">Cricetinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003412" MajorTopicYN="N">Cricetulus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D036145" MajorTopicYN="N">Ginsenosides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019267" MajorTopicYN="N">Hemagglutinin Glycoproteins, Influenza Virus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061985" MajorTopicYN="N">Madin Darby Canine Kidney Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>06</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>01</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>2</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28187149</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0171936</ArticleId><ArticleId IdType="pii">PONE-D-16-25874</ArticleId><ArticleId IdType="pmc">PMC5302443</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Evid Based Complement 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