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Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs

(2010) PLOS ONE. 5(2).
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Abstract
The declaration of the human influenza A pandemic (H1N1) 2009 (H1N1/09) raised important questions, including origin and host range [1,2]. Two of the three pandemics in the last century resulted in the spread of virus to pigs (H1N1, 1918; H3N2, 1968) with subsequent independent establishment and evolution within swine worldwide [3]. A key public and veterinary health consideration in the context of the evolving pandemic is whether the H1N1/09 virus could become established in pig populations [4]. We performed an infection and transmission study in pigs with A/California/07/09. In combination, clinical, pathological, modified influenza A matrix gene real time RT-PCR and viral genomic analyses have shown that infection results in the induction of clinical signs, viral pathogenesis restricted to the respiratory tract, infection dynamics consistent with endemic strains of influenza A in pigs, virus transmissibility between pigs and virus-host adaptation events. Our results demonstrate that extant H1N1/09 is fully capable of becoming established in global pig populations. We also show the roles of viral receptor specificity in both transmission and tissue tropism. Remarkably, following direct inoculation of pigs with virus quasispecies differing by amino acid substitutions in the haemagglutinin receptor-binding site, only virus with aspartic acid at position 225 (225D) was detected in nasal secretions of contact infected pigs. In contrast, in lower respiratory tract samples from directly inoculated pigs, with clearly demonstrable pulmonary pathology, there was apparent selection of a virus variant with glycine (225G). These findings provide potential clues to the existence and biological significance of viral receptor-binding variants with 225D and 225G during the 1918 pandemic [5].
Keywords
C-REACTIVE PROTEIN, INTERSPECIES TRANSMISSION, RECEPTOR-BINDING PROPERTIES, ACUTE-PHASE PROTEIN, AVIAN INFLUENZA-VIRUSES, EXPERIMENTAL-INFECTION, MDCK CELLS, HEMAGGLUTININ, STRAINS, FERRETS

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Citation

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Chicago
Brookes, Sharon M, Alejandro Nunez, Bhudipa Choudhury, Mikhail Matrosovich, Stephen C Essen, Derek Clifford, Marek J Slomka, et al. 2010. “Replication, Pathogenesis and Transmission of Pandemic (H1N1) 2009 Virus in Non-immune Pigs.” Plos One 5 (2).
APA
Brookes, S. M., Nunez, A., Choudhury, B., Matrosovich, M., Essen, S. C., Clifford, D., Slomka, M. J., et al. (2010). Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs. PLOS ONE, 5(2).
Vancouver
1.
Brookes SM, Nunez A, Choudhury B, Matrosovich M, Essen SC, Clifford D, et al. Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs. PLOS ONE. 2010;5(2).
MLA
Brookes, Sharon M, Alejandro Nunez, Bhudipa Choudhury, et al. “Replication, Pathogenesis and Transmission of Pandemic (H1N1) 2009 Virus in Non-immune Pigs.” PLOS ONE 5.2 (2010): n. pag. Print.
@article{1150966,
  abstract     = {The declaration of the human influenza A pandemic (H1N1) 2009 (H1N1/09) raised important questions, including origin and host range [1,2]. Two of the three pandemics in the last century resulted in the spread of virus to pigs (H1N1, 1918; H3N2, 1968) with subsequent independent establishment and evolution within swine worldwide [3]. A key public and veterinary health consideration in the context of the evolving pandemic is whether the H1N1/09 virus could become established in pig populations [4]. We performed an infection and transmission study in pigs with A/California/07/09. In combination, clinical, pathological, modified influenza A matrix gene real time RT-PCR and viral genomic analyses have shown that infection results in the induction of clinical signs, viral pathogenesis restricted to the respiratory tract, infection dynamics consistent with endemic strains of influenza A in pigs, virus transmissibility between pigs and virus-host adaptation events. Our results demonstrate that extant H1N1/09 is fully capable of becoming established in global pig populations. We also show the roles of viral receptor specificity in both transmission and tissue tropism. Remarkably, following direct inoculation of pigs with virus quasispecies differing by amino acid substitutions in the haemagglutinin receptor-binding site, only virus with aspartic acid at position 225 (225D) was detected in nasal secretions of contact infected pigs. In contrast, in lower respiratory tract samples from directly inoculated pigs, with clearly demonstrable pulmonary pathology, there was apparent selection of a virus variant with glycine (225G). These findings provide potential clues to the existence and biological significance of viral receptor-binding variants with 225D and 225G during the 1918 pandemic [5].},
  articleno    = {e9068},
  author       = {Brookes, Sharon M and Nunez, Alejandro and Choudhury, Bhudipa and Matrosovich, Mikhail and Essen, Stephen C and Clifford, Derek and Slomka, Marek J and Kuntz-Simon, Gaelle and Garcon, Fanny and Nash, Bethany and Hanna, Amanda and Heegaard, Peter MH and Queguiner, Stephane and Chiapponi, Chiara and Bublot, Michel and Garcia, Jaime M and Gardner, Rebecca and Foni, Emanuela and Loeffen, Willie and Larsen, Lars and Van Reeth, Kristien and Banks, Jill and Irvine, Richard M and Brown, Ian H},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keyword      = {C-REACTIVE PROTEIN,INTERSPECIES TRANSMISSION,RECEPTOR-BINDING PROPERTIES,ACUTE-PHASE PROTEIN,AVIAN INFLUENZA-VIRUSES,EXPERIMENTAL-INFECTION,MDCK CELLS,HEMAGGLUTININ,STRAINS,FERRETS},
  language     = {eng},
  number       = {2},
  pages        = {9},
  title        = {Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs},
  url          = {http://dx.doi.org/10.1371/journal.pone.0009068},
  volume       = {5},
  year         = {2010},
}

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