PandemieGrippaleV1, PascalFrancis, Curation, bibRecord, 001D88

Intranasal seasonal influenza vaccine and a TLR-3 agonist, rintatolimod, induced cross-reactive IgA antibody formation against avian H5N1 and H7N9 influenza HA in humans

Identifieur interne : 001D88 ( PascalFrancis/Curation ); précédent : 001D87; suivant : 001D89

Intranasal seasonal influenza vaccine and a TLR-3 agonist, rintatolimod, induced cross-reactive IgA antibody formation against avian H5N1 and H7N9 influenza HA in humans

Auteurs : Edgar Turner Overton [États-Unis] ; Paul A. Goepfert [États-Unis] ; Pamela Cunningham [États-Unis] ; William A. Carter [États-Unis] ; Joseph Horvath [États-Unis] ; Diane Young [États-Unis] ; David R. Strayer [États-Unis]

Source :

Vaccine [ 0264-410X ] ; 2014.

RBID : Pascal:14-0246270

Descripteurs français

Pascal (Inist)
- Virus grippal A, Homme, Voie intranasale, Vaccin, IgA, Anticorps, Souche atténuée, Adjuvant immunologique, Muqueuse, Grippe A, Grippe aviaire.
Wicri :
- topic : Homme, Vaccin.

English descriptors

KwdEn :
- Antibody, Attenuated strain, Avian influenza, Human, IgA, Immunological adjuvant, Influenza A, Influenza A virus, Intranasal administration, Mucosa, Vaccine.

Abstract

The intranasal use of rintatolimod, a specific TLR-3 agonist, combined with trivalent seasonal influenza vaccine generated cross-protection against highly pathogenic H5N1 avian influenza in mice. The purpose of this clinical trial is to assess the safety and impact of rintatolimod on intranasal influenza vaccine in healthy adults. During Stage I of this Phase I/II clinical trial, 12 volunteers were immunized intranasally with 3 doses of FluMist® seasonal influenza vaccine on Days 0, 28, and 56 followed by intranasal rintatolimod (50 μg, 200 μg, or 500 μg) 3 days later. Parotid saliva and nasal wash samples were collected at baseline and on Days 25, 53, 84, and 417. The samples were tested for IgA and IgG specific antibodies (Ab) directed against the homologous FluMist® viral hemagglutinins (HAs). In addition, viral specific responses against influenza A HAs were tested for IgA Ab cross-reactivity against 3 H5 clades: HA (H5N1) A/Indonesia/5/2005, HA (H5N1) A/Hong Kong/483/97 and HA (H5N1) A/Vietnam/1194/2004, as well as, two H7 strains, HA (H7N9) A/Shanghai/2/2013 and HA (H7N3) A/chicken/Jalisco/CPA1. The combination of the intranasal FluMist® along with the rintatolimod generated specific secretory IgA responses of at least 4-fold over baseline against at least one of the homologous vaccine strains included in the vaccine in 92% of the vaccinees. Additionally, this vaccination strategy induced cross-reactive secretory IgA against highly pathogenic avian influenza virus strains H5N1, H7N9, and H7N3 with pandemic potential for humans. The combination of rintatolimod and FluMist® was well-tolerated.

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C03	`05`	`X`	`SPA`	`@0 IgA @5 07`
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C03	`06`	`X`	`SPA`	`@0 Anticuerpo @5 08`
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C07	`02`	`X`	`SPA`	`@0 Orthomyxoviridae @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
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C07	`04`	`X`	`ENG`	`@0 Infection @5 13`
C07	`04`	`X`	`SPA`	`@0 Infección @5 13`
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C07	`05`	`X`	`SPA`	`@0 Virosis`
N21				`@1 300`
N44	`01`			`@1 OTO`
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Pascal:14-0246270

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Intranasal seasonal influenza vaccine and a TLR-3 agonist, rintatolimod, induced cross-reactive IgA antibody formation against avian H5N1 and H7N9 influenza HA in humans</title>
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<author><name sortKey="Horvath, Joseph" sort="Horvath, Joseph" uniqKey="Horvath J" first="Joseph" last="Horvath">Joseph Horvath</name>
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<term>Immunological adjuvant</term>
<term>Influenza A</term>
<term>Influenza A virus</term>
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<front><div type="abstract" xml:lang="en">The intranasal use of rintatolimod, a specific TLR-3 agonist, combined with trivalent seasonal influenza vaccine generated cross-protection against highly pathogenic H5N1 avian influenza in mice. The purpose of this clinical trial is to assess the safety and impact of rintatolimod on intranasal influenza vaccine in healthy adults. During Stage I of this Phase I/II clinical trial, 12 volunteers were immunized intranasally with 3 doses of FluMist® seasonal influenza vaccine on Days 0, 28, and 56 followed by intranasal rintatolimod (50 μg, 200 μg, or 500 μg) 3 days later. Parotid saliva and nasal wash samples were collected at baseline and on Days 25, 53, 84, and 417. The samples were tested for IgA and IgG specific antibodies (Ab) directed against the homologous FluMist® viral hemagglutinins (HAs). In addition, viral specific responses against influenza A HAs were tested for IgA Ab cross-reactivity against 3 H5 clades: HA (H5N1) A/Indonesia/5/2005, HA (H5N1) A/Hong Kong/483/97 and HA (H5N1) A/Vietnam/1194/2004, as well as, two H7 strains, HA (H7N9) A/Shanghai/2/2013 and HA (H7N3) A/chicken/Jalisco/CPA1. The combination of the intranasal FluMist® along with the rintatolimod generated specific secretory IgA responses of at least 4-fold over baseline against at least one of the homologous vaccine strains included in the vaccine in 92% of the vaccinees. Additionally, this vaccination strategy induced cross-reactive secretory IgA against highly pathogenic avian influenza virus strains H5N1, H7N9, and H7N3 with pandemic potential for humans. The combination of rintatolimod and FluMist® was well-tolerated.</div>
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<sZ>3 aut.</sZ>
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<fA14 i1="02"><s1>Hemispherx Biopharma, Inc., One Penn Center, 1617JFK Boulevard, Suite 500</s1>
<s2>Philadelphia, PA 19103</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>5490-5495</s1>
</fA20>
<fA21><s1>2014</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20289</s2>
<s5>354000504533570190</s5>
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<s1>© 2014 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>19 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>14-0246270</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Vaccine</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>The intranasal use of rintatolimod, a specific TLR-3 agonist, combined with trivalent seasonal influenza vaccine generated cross-protection against highly pathogenic H5N1 avian influenza in mice. The purpose of this clinical trial is to assess the safety and impact of rintatolimod on intranasal influenza vaccine in healthy adults. During Stage I of this Phase I/II clinical trial, 12 volunteers were immunized intranasally with 3 doses of FluMist® seasonal influenza vaccine on Days 0, 28, and 56 followed by intranasal rintatolimod (50 μg, 200 μg, or 500 μg) 3 days later. Parotid saliva and nasal wash samples were collected at baseline and on Days 25, 53, 84, and 417. The samples were tested for IgA and IgG specific antibodies (Ab) directed against the homologous FluMist® viral hemagglutinins (HAs). In addition, viral specific responses against influenza A HAs were tested for IgA Ab cross-reactivity against 3 H5 clades: HA (H5N1) A/Indonesia/5/2005, HA (H5N1) A/Hong Kong/483/97 and HA (H5N1) A/Vietnam/1194/2004, as well as, two H7 strains, HA (H7N9) A/Shanghai/2/2013 and HA (H7N3) A/chicken/Jalisco/CPA1. The combination of the intranasal FluMist® along with the rintatolimod generated specific secretory IgA responses of at least 4-fold over baseline against at least one of the homologous vaccine strains included in the vaccine in 92% of the vaccinees. Additionally, this vaccination strategy induced cross-reactive secretory IgA against highly pathogenic avian influenza virus strains H5N1, H7N9, and H7N3 with pandemic potential for humans. The combination of rintatolimod and FluMist® was well-tolerated.</s0>
</fC01>
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<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>01</s5>
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<fC03 i1="02" i2="X" l="FRE"><s0>Homme</s0>
<s5>02</s5>
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<s5>02</s5>
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<fC03 i1="02" i2="X" l="SPA"><s0>Hombre</s0>
<s5>02</s5>
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<s5>05</s5>
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<s5>05</s5>
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<s5>05</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Vaccin</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Vaccine</s0>
<s5>06</s5>
</fC03>
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<s5>06</s5>
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<s5>07</s5>
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<s5>07</s5>
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<fC03 i1="05" i2="X" l="SPA"><s0>IgA</s0>
<s5>07</s5>
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<s5>08</s5>
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<fC03 i1="06" i2="X" l="ENG"><s0>Antibody</s0>
<s5>08</s5>
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<fC03 i1="06" i2="X" l="SPA"><s0>Anticuerpo</s0>
<s5>08</s5>
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<fC03 i1="07" i2="X" l="FRE"><s0>Souche atténuée</s0>
<s5>09</s5>
</fC03>
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<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Cepa atenuada</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Adjuvant immunologique</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Immunological adjuvant</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Coadyuvante inmunológico</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Muqueuse</s0>
<s5>11</s5>
</fC03>
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<s5>11</s5>
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<fC03 i1="09" i2="X" l="SPA"><s0>Mucosa</s0>
<s5>11</s5>
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<fC03 i1="10" i2="X" l="FRE"><s0>Grippe A</s0>
<s5>14</s5>
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<fC03 i1="10" i2="X" l="ENG"><s0>Influenza A</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Gripe A</s0>
<s5>14</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Grippe aviaire</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Avian influenza</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Gripe aviar</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Infection</s0>
<s5>13</s5>
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<fC07 i1="04" i2="X" l="ENG"><s0>Infection</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Infección</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fN21><s1>300</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
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Intranasal seasonal influenza vaccine and a TLR-3 agonist, rintatolimod, induced cross-reactive IgA antibody formation against avian H5N1 and H7N9 influenza HA in humans

Intranasal seasonal influenza vaccine and a TLR-3 agonist, rintatolimod, induced cross-reactive IgA antibody formation against avian H5N1 and H7N9 influenza HA in humans

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