Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.
Identifieur interne : 000114 ( Ncbi/Merge ); précédent : 000113; suivant : 000115Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.
Auteurs : M L Clements [États-Unis] ; E K Subbarao ; L F Fries ; R A Karron ; W T London ; B R MurphySource :
- Journal of clinical microbiology [ 0095-1137 ] ; 1992.
Descripteurs français
- KwdFr :
- ARN viral (génétique), Adulte, Animaux, Données de séquences moléculaires, Gènes viraux, Humains, Réplication virale (génétique), Saimiri, Séquence nucléotidique, Transfection, Vaccins antigrippaux (isolement et purification), Vaccins atténués (isolement et purification), Virulence (génétique), Virus de la grippe A (génétique), Virus de la grippe A (pathogénicité), Virus de la grippe A (physiologie).
- MESH :
- génétique : ARN viral, Réplication virale, Virulence, Virus de la grippe A.
- isolement et purification : Vaccins antigrippaux, Vaccins atténués.
- pathogénicité : Virus de la grippe A.
- physiologie : Virus de la grippe A.
- Adulte, Animaux, Données de séquences moléculaires, Gènes viraux, Humains, Saimiri, Séquence nucléotidique, Transfection.
English descriptors
- KwdEn :
- Adult, Animals, Base Sequence, Genes, Viral, Humans, Influenza A virus (genetics), Influenza A virus (pathogenicity), Influenza A virus (physiology), Influenza Vaccines (isolation & purification), Molecular Sequence Data, RNA, Viral (genetics), Saimiri, Transfection, Vaccines, Attenuated (isolation & purification), Virulence (genetics), Virus Replication (genetics).
- MESH :
- chemical , genetics : RNA, Viral.
- chemical , isolation & purification : Influenza Vaccines, Vaccines, Attenuated.
- genetics : Influenza A virus, Virulence, Virus Replication.
- pathogenicity : Influenza A virus.
- physiology : Influenza A virus.
- Adult, Animals, Base Sequence, Genes, Viral, Humans, Molecular Sequence Data, Saimiri, Transfection.
Abstract
The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P less than 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus specified restriction of virus replication in humans.
PubMed: 1551982
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Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Subbarao, E K" sort="Subbarao, E K" uniqKey="Subbarao E" first="E K" last="Subbarao">E K Subbarao</name></author><author><name sortKey="Fries, L F" sort="Fries, L F" uniqKey="Fries L" first="L F" last="Fries">L F Fries</name></author><author><name sortKey="Karron, R A" sort="Karron, R A" uniqKey="Karron R" first="R A" last="Karron">R A Karron</name></author><author><name sortKey="London, W T" sort="London, W T" uniqKey="London W" first="W T" last="London">W T London</name></author><author><name sortKey="Murphy, B R" sort="Murphy, B R" uniqKey="Murphy B" first="B R" last="Murphy">B R Murphy</name></author></analytic><series><title level="j">Journal of clinical microbiology</title><idno type="ISSN">0095-1137</idno><imprint><date when="1992" type="published">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Animals</term><term>Base Sequence</term><term>Genes, Viral</term><term>Humans</term><term>Influenza A virus (genetics)</term><term>Influenza A virus (pathogenicity)</term><term>Influenza A virus (physiology)</term><term>Influenza Vaccines (isolation & purification)</term><term>Molecular Sequence Data</term><term>RNA, Viral (genetics)</term><term>Saimiri</term><term>Transfection</term><term>Vaccines, Attenuated (isolation & purification)</term><term>Virulence (genetics)</term><term>Virus Replication (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (génétique)</term><term>Adulte</term><term>Animaux</term><term>Données de séquences moléculaires</term><term>Gènes viraux</term><term>Humains</term><term>Réplication virale (génétique)</term><term>Saimiri</term><term>Séquence nucléotidique</term><term>Transfection</term><term>Vaccins antigrippaux (isolement et purification)</term><term>Vaccins atténués (isolement et purification)</term><term>Virulence (génétique)</term><term>Virus de la grippe A (génétique)</term><term>Virus de la grippe A (pathogénicité)</term><term>Virus de la grippe A (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="isolation & purification" xml:lang="en"><term>Influenza Vaccines</term><term>Vaccines, Attenuated</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A virus</term><term>Virulence</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN viral</term><term>Réplication virale</term><term>Virulence</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Vaccins antigrippaux</term><term>Vaccins atténués</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Animals</term><term>Base Sequence</term><term>Genes, Viral</term><term>Humans</term><term>Molecular Sequence Data</term><term>Saimiri</term><term>Transfection</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Animaux</term><term>Données de séquences moléculaires</term><term>Gènes viraux</term><term>Humains</term><term>Saimiri</term><term>Séquence nucléotidique</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P less than 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus specified restriction of virus replication in humans.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1551982</PMID><DateCompleted><Year>1992</Year><Month>04</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0095-1137</ISSN><JournalIssue CitedMedium="Print"><Volume>30</Volume><Issue>3</Issue><PubDate><Year>1992</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of clinical microbiology</Title><ISOAbbreviation>J. Clin. Microbiol.</ISOAbbreviation></Journal><ArticleTitle>Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.</ArticleTitle><Pagination><MedlinePgn>655-62</MedlinePgn></Pagination><Abstract><AbstractText>The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P less than 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus specified restriction of virus replication in humans.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Clements</LastName><ForeName>M L</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Department of International Health, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Subbarao</LastName><ForeName>E K</ForeName><Initials>EK</Initials></Author><Author ValidYN="Y"><LastName>Fries</LastName><ForeName>L F</ForeName><Initials>LF</Initials></Author><Author ValidYN="Y"><LastName>Karron</LastName><ForeName>R A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>London</LastName><ForeName>W T</ForeName><Initials>WT</Initials></Author><Author ValidYN="Y"><LastName>Murphy</LastName><ForeName>B R</ForeName><Initials>BR</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01 AI 62515</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Microbiol</MedlineTA><NlmUniqueID>7505564</NlmUniqueID><ISSNLinking>0095-1137</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007252">Influenza Vaccines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">Influenza Vaccines</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012367" MajorTopicYN="N">RNA, Viral</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012453" MajorTopicYN="N">Saimiri</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014613" MajorTopicYN="N">Vaccines, Attenuated</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>3</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1551982</ArticleId><ArticleId IdType="pmc">PMC265127</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Clin Microbiol. 1986 May;23(5):852-7</Citation><ArticleIdList><ArticleId 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