Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses
Identifieur interne : 000004 ( PascalFrancis/Corpus ); précédent : 000003; suivant : 000005Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses
Auteurs : Jens C. Krause ; Tshidi Tsibane ; Terrence M. Tumpey ; Chelsey J. Huffman ; Randy Albrecht ; David L. Blum ; Irene Ramos ; Ana Fernandez-Sesma ; Kathryn M. Edwards ; Adolfo Garcia-Sastre ; Christopher F. Basler ; James E. Jr CroweSource :
- Journal of virology [ 0022-538X ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Investigation of the human antibody response to the 1957 pandemic H2N2 influenza A virus has been largely limited to serologic studies. We generated five influenza virus hemagglutinin (HA)-reactive human monoclonal antibodies (MAbs) by hybridoma technology from the peripheral blood of healthy donors who were born between 1950 and 1968. Two MAbs reacted with the pandemic H2N2 virus, two recognized the pandemic H3N2 virus, and remarkably, one reacted with both the pandemic H2N2 and H3N2 viruses. Each of these five naturally occurring MAbs displayed hemagglutination inhibition activity, suggesting specificity for the globular head domain of influenza virus HA. When incubated with virus, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-binding domain on the HA globular head in embryonated chicken eggs. All H2N2-specific MAbs were able to inhibit a 2006 swine H2N3 influenza virus. MAbs 8M2 and 2G1 shared the VH1-69 germ line gene, but these antibodies were otherwise not genetically related. Each antibody was able to protect mice in a lethal H2N2 virus challenge. Thus, even 43 years after circulation of H2N2 viruses, these subjects possessed peripheral blood B cells encoding potent inhibiting antibodies specific for a conserved region on the globular head of the pandemic H2 HA.
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Format Inist (serveur)
| NO : | PASCAL 12-0227810 INIST |
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| ET : | Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses |
| AU : | KRAUSE (Jens C.); TSIBANE (Tshidi); TUMPEY (Terrence M.); HUFFMAN (Chelsey J.); ALBRECHT (Randy); BLUM (David L.); RAMOS (Irene); FERNANDEZ-SESMA (Ana); EDWARDS (Kathryn M.); GARCIA-SASTRE (Adolfo); BASLER (Christopher F.); CROWE (James E. JR) |
| AF : | Department of Pediatrics, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 4 aut., 6 aut., 9 aut., 12 aut.); Department of Microbiology and Immunology, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (12 aut.); Department of Microbiology, Mount Sinai School of Medicine/New York, New York/Etats-Unis (2 aut., 5 aut., 7 aut., 8 aut., 10 aut., 11 aut.); Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine/New York, New York/Etats-Unis (8 aut., 10 aut.); Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine/New York, New York/Etats-Unis (5 aut., 8 aut., 10 aut.); Influenza Division, Centers for Disease Control and Prevention/Atlanta, Georgia/Etats-Unis (3 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 11; Pp. 6334-6340; Bibl. 54 ref. |
| LA : | Anglais |
| EA : | Investigation of the human antibody response to the 1957 pandemic H2N2 influenza A virus has been largely limited to serologic studies. We generated five influenza virus hemagglutinin (HA)-reactive human monoclonal antibodies (MAbs) by hybridoma technology from the peripheral blood of healthy donors who were born between 1950 and 1968. Two MAbs reacted with the pandemic H2N2 virus, two recognized the pandemic H3N2 virus, and remarkably, one reacted with both the pandemic H2N2 and H3N2 viruses. Each of these five naturally occurring MAbs displayed hemagglutination inhibition activity, suggesting specificity for the globular head domain of influenza virus HA. When incubated with virus, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-binding domain on the HA globular head in embryonated chicken eggs. All H2N2-specific MAbs were able to inhibit a 2006 swine H2N3 influenza virus. MAbs 8M2 and 2G1 shared the VH1-69 germ line gene, but these antibodies were otherwise not genetically related. Each antibody was able to protect mice in a lethal H2N2 virus challenge. Thus, even 43 years after circulation of H2N2 viruses, these subjects possessed peripheral blood B cells encoding potent inhibiting antibodies specific for a conserved region on the globular head of the pandemic H2 HA. |
| CC : | 002A05C10; 002A05C07 |
| FD : | Homme; Anticorps monoclonal; Grippe |
| FG : | Virose; Infection |
| ED : | Human; Monoclonal antibody; Influenza |
| EG : | Viral disease; Infection |
| SD : | Hombre; Anticuerpo monoclonal; Gripe |
| LO : | INIST-13592.354000509353530340 |
| ID : | 12-0227810 |
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Pascal:12-0227810Le document en format XML
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Jr Crowe</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Microbiology and Immunology, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>12 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0227810</idno><date when="2012">2012</date><idno type="stanalyst">PASCAL 12-0227810 INIST</idno><idno type="RBID">Pascal:12-0227810</idno><idno type="wicri:Area/PascalFrancis/Corpus">000004</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses</title><author><name sortKey="Krause, Jens C" sort="Krause, Jens C" uniqKey="Krause J" first="Jens C." last="Krause">Jens C. Krause</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tsibane, Tshidi" sort="Tsibane, Tshidi" uniqKey="Tsibane T" first="Tshidi" last="Tsibane">Tshidi Tsibane</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M." last="Tumpey">Terrence M. Tumpey</name><affiliation><inist:fA14 i1="06"><s1>Influenza Division, Centers for Disease Control and Prevention</s1><s2>Atlanta, Georgia</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Huffman, Chelsey J" sort="Huffman, Chelsey J" uniqKey="Huffman C" first="Chelsey J." last="Huffman">Chelsey J. Huffman</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Albrecht, Randy" sort="Albrecht, Randy" uniqKey="Albrecht R" first="Randy" last="Albrecht">Randy Albrecht</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Blum, David L" sort="Blum, David L" uniqKey="Blum D" first="David L." last="Blum">David L. Blum</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ramos, Irene" sort="Ramos, Irene" uniqKey="Ramos I" first="Irene" last="Ramos">Irene Ramos</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fernandez Sesma, Ana" sort="Fernandez Sesma, Ana" uniqKey="Fernandez Sesma A" first="Ana" last="Fernandez-Sesma">Ana Fernandez-Sesma</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Edwards, Kathryn M" sort="Edwards, Kathryn M" uniqKey="Edwards K" first="Kathryn M." last="Edwards">Kathryn M. Edwards</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Garcia Sastre, Adolfo" sort="Garcia Sastre, Adolfo" uniqKey="Garcia Sastre A" first="Adolfo" last="Garcia-Sastre">Adolfo Garcia-Sastre</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Basler, Christopher F" sort="Basler, Christopher F" uniqKey="Basler C" first="Christopher F." last="Basler">Christopher F. Basler</name><affiliation><inist:fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Crowe, James E Jr" sort="Crowe, James E Jr" uniqKey="Crowe J" first="James E. Jr" last="Crowe">James E. Jr Crowe</name><affiliation><inist:fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Microbiology and Immunology, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>12 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Human</term><term>Influenza</term><term>Monoclonal antibody</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Homme</term><term>Anticorps monoclonal</term><term>Grippe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Investigation of the human antibody response to the 1957 pandemic H2N2 influenza A virus has been largely limited to serologic studies. We generated five influenza virus hemagglutinin (HA)-reactive human monoclonal antibodies (MAbs) by hybridoma technology from the peripheral blood of healthy donors who were born between 1950 and 1968. Two MAbs reacted with the pandemic H2N2 virus, two recognized the pandemic H3N2 virus, and remarkably, one reacted with both the pandemic H2N2 and H3N2 viruses. Each of these five naturally occurring MAbs displayed hemagglutination inhibition activity, suggesting specificity for the globular head domain of influenza virus HA. When incubated with virus, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-binding domain on the HA globular head in embryonated chicken eggs. All H2N2-specific MAbs were able to inhibit a 2006 swine H2N3 influenza virus. MAbs 8M2 and 2G1 shared the V<sub>H</sub>1-69 germ line gene, but these antibodies were otherwise not genetically related. Each antibody was able to protect mice in a lethal H2N2 virus challenge. Thus, even 43 years after circulation of H2N2 viruses, these subjects possessed peripheral blood B cells encoding potent inhibiting antibodies specific for a conserved region on the globular head of the pandemic H2 HA.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-538X</s0></fA01><fA03 i2="1"><s0>J. virol.</s0></fA03><fA05><s2>86</s2></fA05><fA06><s2>11</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses</s1></fA08><fA11 i1="01" i2="1"><s1>KRAUSE (Jens C.)</s1></fA11><fA11 i1="02" i2="1"><s1>TSIBANE (Tshidi)</s1></fA11><fA11 i1="03" i2="1"><s1>TUMPEY (Terrence M.)</s1></fA11><fA11 i1="04" i2="1"><s1>HUFFMAN (Chelsey J.)</s1></fA11><fA11 i1="05" i2="1"><s1>ALBRECHT (Randy)</s1></fA11><fA11 i1="06" i2="1"><s1>BLUM (David L.)</s1></fA11><fA11 i1="07" i2="1"><s1>RAMOS (Irene)</s1></fA11><fA11 i1="08" i2="1"><s1>FERNANDEZ-SESMA (Ana)</s1></fA11><fA11 i1="09" i2="1"><s1>EDWARDS (Kathryn M.)</s1></fA11><fA11 i1="10" i2="1"><s1>GARCIA-SASTRE (Adolfo)</s1></fA11><fA11 i1="11" i2="1"><s1>BASLER (Christopher F.)</s1></fA11><fA11 i1="12" i2="1"><s1>CROWE (James E. JR)</s1></fA11><fA14 i1="01"><s1>Department of Pediatrics, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Microbiology and Immunology, Vanderbilt University Medical Center</s1><s2>Nashville, Tennessee</s2><s3>USA</s3><sZ>12 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Microbiology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>10 aut.</sZ></fA14><fA14 i1="05"><s1>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>10 aut.</sZ></fA14><fA14 i1="06"><s1>Influenza Division, Centers for Disease Control and Prevention</s1><s2>Atlanta, Georgia</s2><s3>USA</s3><sZ>3 aut.</sZ></fA14><fA20><s1>6334-6340</s1></fA20><fA21><s1>2012</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>13592</s2><s5>354000509353530340</s5></fA43><fA44><s0>0000</s0><s1>© 2012 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>54 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>12-0227810</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of virology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Investigation of the human antibody response to the 1957 pandemic H2N2 influenza A virus has been largely limited to serologic studies. We generated five influenza virus hemagglutinin (HA)-reactive human monoclonal antibodies (MAbs) by hybridoma technology from the peripheral blood of healthy donors who were born between 1950 and 1968. Two MAbs reacted with the pandemic H2N2 virus, two recognized the pandemic H3N2 virus, and remarkably, one reacted with both the pandemic H2N2 and H3N2 viruses. Each of these five naturally occurring MAbs displayed hemagglutination inhibition activity, suggesting specificity for the globular head domain of influenza virus HA. When incubated with virus, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-binding domain on the HA globular head in embryonated chicken eggs. All H2N2-specific MAbs were able to inhibit a 2006 swine H2N3 influenza virus. MAbs 8M2 and 2G1 shared the V<sub>H</sub>1-69 germ line gene, but these antibodies were otherwise not genetically related. Each antibody was able to protect mice in a lethal H2N2 virus challenge. Thus, even 43 years after circulation of H2N2 viruses, these subjects possessed peripheral blood B cells encoding potent inhibiting antibodies specific for a conserved region on the globular head of the pandemic H2 HA.</s0></fC01><fC02 i1="01" i2="X"><s0>002A05C10</s0></fC02><fC02 i1="02" i2="X"><s0>002A05C07</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Homme</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Human</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Hombre</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Anticorps monoclonal</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Monoclonal antibody</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Anticuerpo monoclonal</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Grippe</s0><s5>14</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Influenza</s0><s5>14</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Gripe</s0><s5>14</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Virose</s0></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0></fC07><fN21><s1>177</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 12-0227810 INIST</NO><ET>Human Monoclonal Antibodies to Pandemic 1957 H2N2 and Pandemic 1968 H3N2 Influenza Viruses</ET><AU>KRAUSE (Jens C.); TSIBANE (Tshidi); TUMPEY (Terrence M.); HUFFMAN (Chelsey J.); ALBRECHT (Randy); BLUM (David L.); RAMOS (Irene); FERNANDEZ-SESMA (Ana); EDWARDS (Kathryn M.); GARCIA-SASTRE (Adolfo); BASLER (Christopher F.); CROWE (James E. JR)</AU><AF>Department of Pediatrics, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 4 aut., 6 aut., 9 aut., 12 aut.); Department of Microbiology and Immunology, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (12 aut.); Department of Microbiology, Mount Sinai School of Medicine/New York, New York/Etats-Unis (2 aut., 5 aut., 7 aut., 8 aut., 10 aut., 11 aut.); Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine/New York, New York/Etats-Unis (8 aut., 10 aut.); Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine/New York, New York/Etats-Unis (5 aut., 8 aut., 10 aut.); Influenza Division, Centers for Disease Control and Prevention/Atlanta, Georgia/Etats-Unis (3 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 11; Pp. 6334-6340; Bibl. 54 ref.</SO><LA>Anglais</LA><EA>Investigation of the human antibody response to the 1957 pandemic H2N2 influenza A virus has been largely limited to serologic studies. We generated five influenza virus hemagglutinin (HA)-reactive human monoclonal antibodies (MAbs) by hybridoma technology from the peripheral blood of healthy donors who were born between 1950 and 1968. Two MAbs reacted with the pandemic H2N2 virus, two recognized the pandemic H3N2 virus, and remarkably, one reacted with both the pandemic H2N2 and H3N2 viruses. Each of these five naturally occurring MAbs displayed hemagglutination inhibition activity, suggesting specificity for the globular head domain of influenza virus HA. When incubated with virus, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-binding domain on the HA globular head in embryonated chicken eggs. All H2N2-specific MAbs were able to inhibit a 2006 swine H2N3 influenza virus. MAbs 8M2 and 2G1 shared the V<sub>H</sub>1-69 germ line gene, but these antibodies were otherwise not genetically related. Each antibody was able to protect mice in a lethal H2N2 virus challenge. Thus, even 43 years after circulation of H2N2 viruses, these subjects possessed peripheral blood B cells encoding potent inhibiting antibodies specific for a conserved region on the globular head of the pandemic H2 HA.</EA><CC>002A05C10; 002A05C07</CC><FD>Homme; Anticorps monoclonal; Grippe</FD><FG>Virose; Infection</FG><ED>Human; Monoclonal antibody; Influenza</ED><EG>Viral disease; Infection</EG><SD>Hombre; Anticuerpo monoclonal; Gripe</SD><LO>INIST-13592.354000509353530340</LO><ID>12-0227810</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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