Literature DB >> 20926110

Classical swine H1N1 influenza viruses confer cross protection from swine-origin 2009 pandemic H1N1 influenza virus infection in mice and ferrets.

Ji-Young Min1, Grace L Chen1, Celia Santos1, Elaine W Lamirande1, Yumiko Matsuoka1, Kanta Subbarao1.   

Abstract

The hemagglutinin of the 2009 pandemic H1N1 influenza virus is a derivative of and is antigenically related to classical swine but not to seasonal human H1N1 viruses. We compared the A/California/7/2009 (CA/7/09) virus recommended by the WHO as the reference virus for vaccine development, with two classical swine influenza viruses A/swine/Iowa/31 (sw/IA/31) and A/New Jersey/8/1976 (NJ/76) to establish the extent of immunologic cross-reactivity and cross-protection in animal models. Primary infection with 2009 pandemic or NJ/76 viruses elicited antibodies against the CA/7/09 virus and provided complete protection from challenge with this virus in ferrets; the response in mice was variable and conferred partial protection. Although ferrets infected with sw/IA/31 virus developed low titers of cross-neutralizing antibody, they were protected from pulmonary replication of the CA/7/09 virus. The data suggest that prior exposure to antigenically related H1N1 viruses of swine-origin provide some protective immunity against the 2009 pandemic H1N1 virus. Published by Elsevier Inc.

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Year:  2010        PMID： 20926110      PMCID： PMC4792254          DOI： 10.1016/j.virol.2010.09.009

Source DB:  PubMed          Journal:  Virology        ISSN： 0042-6822            Impact factor:   3.616


  30 in total

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5.  Outbreak of swine-origin influenza A (H1N1) virus infection - Mexico, March-April 2009.

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Journal:  MMWR Morb Mortal Wkly Rep       Date:  2009-05-08       Impact factor: 17.586

6.  Prior infection with classical swine H1N1 influenza viruses is associated with protective immunity to the 2009 pandemic H1N1 virus.

Authors:  John C Kash; Li Qi; Vivien G Dugan; Brett W Jagger; Rachel J Hrabal; Matthew J Memoli; David M Morens; Jeffery K Taubenberger
Journal:  Influenza Other Respir Viruses       Date:  2010-05-01       Impact factor: 4.380

7.  Pathogenesis and transmission of swine-origin 2009 A(H1N1) influenza virus in ferrets.

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8.  Triple-reassortant swine influenza A (H1) in humans in the United States, 2005-2009.

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10.  Swine influenza A at Fort Dix, New Jersey (January-February 1976). III. Extent of spread and duration of the outbreak.

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Journal:  J Infect Dis       Date:  1977-12       Impact factor: 5.226
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  18 in total

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2.  Eurasian-origin gene segments contribute to the transmissibility, aerosol release, and morphology of the 2009 pandemic H1N1 influenza virus.

Authors:  Seema S Lakdawala; Elaine W Lamirande; Amorsolo L Suguitan; Weijia Wang; Celia P Santos; Leatrice Vogel; Yumiko Matsuoka; William G Lindsley; Hong Jin; Kanta Subbarao
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3.  Severity of clinical disease and pathology in ferrets experimentally infected with influenza viruses is influenced by inoculum volume.

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4.  Receptor specificity does not affect replication or virulence of the 2009 pandemic H1N1 influenza virus in mice and ferrets.

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5.  Infection with seasonal influenza virus elicits CD4 T cells specific for genetically conserved epitopes that can be rapidly mobilized for protective immunity to pandemic H1N1 influenza virus.

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10.  Humans and ferrets with prior H1N1 influenza virus infections do not exhibit evidence of original antigenic sin after infection or vaccination with the 2009 pandemic H1N1 influenza virus.

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