SrasV1, PascalFrancis, Curation, bibRecord, 000944

Intranasal Treatment with Poly(I.C) Protects Aged Mice from Lethal Respiratory Virus Infections

Identifieur interne : 000944 ( PascalFrancis/Curation ); précédent : 000943; suivant : 000945

Intranasal Treatment with Poly(I.C) Protects Aged Mice from Lethal Respiratory Virus Infections

Auteurs : JINCUN ZHAO [États-Unis] ; Christine Wohlford-Lenane [États-Unis] ; JINGXIAN ZHAO [États-Unis, République populaire de Chine] ; Erica Fleming [États-Unis] ; Thomas E. Lane [États-Unis] ; Paul B. Jr Mccray [États-Unis] ; Stanley Perlman [États-Unis]

Source :

Journal of virology [ 0022-538X ] ; 2012.

RBID : Pascal:12-0409934

Descripteurs français

Pascal (Inist)
- Souris, Voie intranasale, Traitement, Pathologie de l'appareil respiratoire, Virose.

English descriptors

KwdEn :
- Intranasal administration, Mouse, Respiratory disease, Treatment, Viral disease.

Abstract

In the 2002-2003 severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic, no patients under 24 years of age died, while mortality was greater than 50% in those over 65 years. Greater than 90% of all deaths from influenza A virus (IAV) occur in the elderly (> 65 years of age). To address this age-related susceptibility to SARS-CoV and IAV, we infected C57BL/6 (B6) mice with mouse-adapted SARS-CoV (MA15) or IAV (PR8), both of which cause severe disease in aged mice. Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a lesser extent, CpG, R848, or lipopolysaccharide (TLR9, TLR7/8, or TLR4 agonists), provided a high level of protection [90% to 100% survival rate after poly(I.C) treatment] against lethal MA15 or IAV challenge and reduced pathological changes and virus loads in the lungs at early times after infection. Poly(I.C) pretreatment upregulated beta interferon (IFN-β), IFN-γ, IL-1β, and tumor necrosis factor (TNF) gene expression in the lungs. Intranasal pretreatment with IFN-β or IFN-γ but not IL-1β or TNF also protected aged mice, consistent with the notion that poly(I.C) pretreatment functioned, at least in part, by inducing IFN-β and IFN-γ. We also identified a potential cellular target for poly(I.C) by showing that treatment inhibited virus replication in primary human airway epithelial cells. These results suggest that intranasal poly(I.C) should be evaluated as a prophylactic agent in aged individuals at high risk for contracting SARS-CoV or IAV infections.

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A03		`1`		`@0 J. virol.`
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A11	`01`	`1`		`@1 JINCUN ZHAO`
A11	`02`	`1`		`@1 WOHLFORD-LENANE (Christine)`
A11	`03`	`1`		`@1 JINGXIAN ZHAO`
A11	`04`	`1`		`@1 FLEMING (Erica)`
A11	`05`	`1`		`@1 LANE (Thomas E.)`
A11	`06`	`1`		`@1 MCCRAY (Paul B. JR)`
A11	`07`	`1`		`@1 PERLMAN (Stanley)`
A14	`01`			`@1 Department of Microbiology, University of Iowa @2 Iowa City, Iowa @3 USA @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 6 aut. @Z 7 aut.`
A14	`02`			`@1 Department of Pediatrics, University of Iowa @2 Iowa City, Iowa @3 USA @Z 2 aut. @Z 6 aut. @Z 7 aut.`
A14	`03`			`@1 Institute for Tissue Transplantation and Immunology, Jinan University @2 Guangzhou @3 CHN @Z 3 aut.`
A14	`04`			`@1 Department of Molecular Biology and Biochemistry, University of California at Irvine @2 Irvine, California @3 USA @Z 5 aut.`
A20				`@1 11416-11424`
A21				`@1 2012`
A23	`01`			`@0 ENG`
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A44				`@0 0000 @1 © 2012 INIST-CNRS. All rights reserved.`
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A47	`01`	`1`		`@0 12-0409934`
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A64	`01`	`1`		`@0 Journal of virology`
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C01	`01`		`ENG`	@0 In the 2002-2003 severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic, no patients under 24 years of age died, while mortality was greater than 50% in those over 65 years. Greater than 90% of all deaths from influenza A virus (IAV) occur in the elderly (> 65 years of age). To address this age-related susceptibility to SARS-CoV and IAV, we infected C57BL/6 (B6) mice with mouse-adapted SARS-CoV (MA15) or IAV (PR8), both of which cause severe disease in aged mice. Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a lesser extent, CpG, R848, or lipopolysaccharide (TLR9, TLR7/8, or TLR4 agonists), provided a high level of protection [90% to 100% survival rate after poly(I.C) treatment] against lethal MA15 or IAV challenge and reduced pathological changes and virus loads in the lungs at early times after infection. Poly(I.C) pretreatment upregulated beta interferon (IFN-β), IFN-γ, IL-1β, and tumor necrosis factor (TNF) gene expression in the lungs. Intranasal pretreatment with IFN-β or IFN-γ but not IL-1β or TNF also protected aged mice, consistent with the notion that poly(I.C) pretreatment functioned, at least in part, by inducing IFN-β and IFN-γ. We also identified a potential cellular target for poly(I.C) by showing that treatment inhibited virus replication in primary human airway epithelial cells. These results suggest that intranasal poly(I.C) should be evaluated as a prophylactic agent in aged individuals at high risk for contracting SARS-CoV or IAV infections.
C02	`01`	`X`		`@0 002A05C10`
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C03	`01`	`X`	`ENG`	`@0 Mouse @5 01`
C03	`01`	`X`	`SPA`	`@0 Ratón @5 01`
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C03	`02`	`X`	`ENG`	`@0 Intranasal administration @5 05`
C03	`02`	`X`	`SPA`	`@0 Vía intranasal @5 05`
C03	`03`	`X`	`FRE`	`@0 Traitement @5 06`
C03	`03`	`X`	`ENG`	`@0 Treatment @5 06`
C03	`03`	`X`	`SPA`	`@0 Tratamiento @5 06`
C03	`04`	`X`	`FRE`	`@0 Pathologie de l'appareil respiratoire @5 07`
C03	`04`	`X`	`ENG`	`@0 Respiratory disease @5 07`
C03	`04`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 07`
C03	`05`	`X`	`FRE`	`@0 Virose @5 14`
C03	`05`	`X`	`ENG`	`@0 Viral disease @5 14`
C03	`05`	`X`	`SPA`	`@0 Virosis @5 14`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`SPA`	`@0 Rodentia @2 NS`
C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`SPA`	`@0 Vertebrata @2 NS`
C07	`04`	`X`	`FRE`	`@0 Infection`
C07	`04`	`X`	`ENG`	`@0 Infection`
C07	`04`	`X`	`SPA`	`@0 Infección`
N21				`@1 317`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Le document en format XML

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<front><div type="abstract" xml:lang="en">In the 2002-2003 severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic, no patients under 24 years of age died, while mortality was greater than 50% in those over 65 years. Greater than 90% of all deaths from influenza A virus (IAV) occur in the elderly (> 65 years of age). To address this age-related susceptibility to SARS-CoV and IAV, we infected C57BL/6 (B6) mice with mouse-adapted SARS-CoV (MA15) or IAV (PR8), both of which cause severe disease in aged mice. Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a lesser extent, CpG, R848, or lipopolysaccharide (TLR9, TLR7/8, or TLR4 agonists), provided a high level of protection [90% to 100% survival rate after poly(I.C) treatment] against lethal MA15 or IAV challenge and reduced pathological changes and virus loads in the lungs at early times after infection. Poly(I.C) pretreatment upregulated beta interferon (IFN-β), IFN-γ, IL-1β, and tumor necrosis factor (TNF) gene expression in the lungs. Intranasal pretreatment with IFN-β or IFN-γ but not IL-1β or TNF also protected aged mice, consistent with the notion that poly(I.C) pretreatment functioned, at least in part, by inducing IFN-β and IFN-γ. We also identified a potential cellular target for poly(I.C) by showing that treatment inhibited virus replication in primary human airway epithelial cells. These results suggest that intranasal poly(I.C) should be evaluated as a prophylactic agent in aged individuals at high risk for contracting SARS-CoV or IAV infections.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Intranasal Treatment with Poly(I.C) Protects Aged Mice from Lethal Respiratory Virus Infections</s1>
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<fA11 i1="01" i2="1"><s1>JINCUN ZHAO</s1>
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<fA14 i1="01"><s1>Department of Microbiology, University of Iowa</s1>
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<fA14 i1="02"><s1>Department of Pediatrics, University of Iowa</s1>
<s2>Iowa City, Iowa</s2>
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<fA14 i1="03"><s1>Institute for Tissue Transplantation and Immunology, Jinan University</s1>
<s2>Guangzhou</s2>
<s3>CHN</s3>
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<fA14 i1="04"><s1>Department of Molecular Biology and Biochemistry, University of California at Irvine</s1>
<s2>Irvine, California</s2>
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<s2>13592</s2>
<s5>354000506814370010</s5>
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<fA44><s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>36 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>12-0409934</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>In the 2002-2003 severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic, no patients under 24 years of age died, while mortality was greater than 50% in those over 65 years. Greater than 90% of all deaths from influenza A virus (IAV) occur in the elderly (> 65 years of age). To address this age-related susceptibility to SARS-CoV and IAV, we infected C57BL/6 (B6) mice with mouse-adapted SARS-CoV (MA15) or IAV (PR8), both of which cause severe disease in aged mice. Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a lesser extent, CpG, R848, or lipopolysaccharide (TLR9, TLR7/8, or TLR4 agonists), provided a high level of protection [90% to 100% survival rate after poly(I.C) treatment] against lethal MA15 or IAV challenge and reduced pathological changes and virus loads in the lungs at early times after infection. Poly(I.C) pretreatment upregulated beta interferon (IFN-β), IFN-γ, IL-1β, and tumor necrosis factor (TNF) gene expression in the lungs. Intranasal pretreatment with IFN-β or IFN-γ but not IL-1β or TNF also protected aged mice, consistent with the notion that poly(I.C) pretreatment functioned, at least in part, by inducing IFN-β and IFN-γ. We also identified a potential cellular target for poly(I.C) by showing that treatment inhibited virus replication in primary human airway epithelial cells. These results suggest that intranasal poly(I.C) should be evaluated as a prophylactic agent in aged individuals at high risk for contracting SARS-CoV or IAV infections.</s0>
</fC01>
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</fC02>
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<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Mouse</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Ratón</s0>
<s5>01</s5>
</fC03>
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<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Intranasal administration</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Vía intranasal</s0>
<s5>05</s5>
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<s5>06</s5>
</fC03>
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<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Tratamiento</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Virose</s0>
<s5>14</s5>
</fC03>
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<s5>14</s5>
</fC03>
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<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fN21><s1>317</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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Intranasal Treatment with Poly(I.C) Protects Aged Mice from Lethal Respiratory Virus Infections

Intranasal Treatment with Poly(I.C) Protects Aged Mice from Lethal Respiratory Virus Infections

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