Advanced search
Add to list

Enhanced pig-to-pig transmission of a reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal genes by serial passaging in pigs

Author
Organization
Project
  • FLUPIG (Pathogenesis and transmission of influenza in pigs (FLUPIG))
Abstract
Avian influenza viruses of H9N2 subtype are endemic in poultry in Asia and the Middle East. Since 1998, they sporadically have caused dead-end infections in humans and swine. Along with avian H7 and H5 influenza viruses, H9N2 is in the top-3 of the world health organization’s list of pandemic influenza virus candidates. On the other hand, the 2009 pandemic H1N1 (pH1N1) virus originated from and has become endemic in swine. Its internal gene cassette has extensively reassorted with established swine influenza viruses all over the world. This pH1N1 internal gene cassette appears to be highly compatible with the surface protein genes of H9N2. This finding has raised concerns about the possible emergence of H9N2 reassortants with public health implications in swine. Moreover, such reassortant viruses showed increased replication and transmissibility in the mouse and ferret model of influenza. The few studies in pigs have also suggested improved fitness of the reassortants as compared to the parental H9N2 virus. We aimed to evaluate if a reassortant H9N2 virus could become better adapted to pigs by serial passaging. To investigate this we performed pig transmission experiments with four different viruses: a reassortant virus containing A/Quail/Hong Kong/G1/97 (H9N2) surface genes and A/California/04/09 (pH1N1) internal genes; another reassortant virus with the same gene constellation that had undergone seven passages in pigs and both parental viruses, H9N2 and pH1N1. Replication efficiency in the porcine lower respiratory tract was minimal for the reassortant H9N2 virus, enhanced for the wholly avian H9N2 virus and greatest for the pig-passaged H9N2 reassortant, with 0, 55 and 93% of the lower respiratory tract samples testing positive for the respective viruses. In pig transmission studies, pH1N1 was excreted in high amounts by all three directly inoculated pigs and six out of six direct contact pigs (mean area under the curve (AUC) for the direct contact pigs of 19,7). In contrast, none of the contact pigs shed high amounts of the parental H9N2 or the original H9N2 reassortant virus (means AUC 3,0 and 4,7, respectively), pointing to inefficient virus transmission. Remarkably, the pig-passaged reassortant was excreted in high titers by four out of six contact animals, with a mean AUC of 16,1. The genetic analysis of the reassortant viruses, to identify which mutations appeared during serial passaging allowing enhanced transmission, is still pending. Our findings confirm that avian H9N2 surface genes are compatible with pH1N1 internal gene cassette, that pigs could serve as suitable intermediate host for the adaptation of reassortant H9N2 virus to mammals, and thus pose a risk of becoming pandemic in humans.

Citation

Please use this url to cite or link to this publication:

MLA
Mancera Gracia, José Carlos, and Kristien Van Reeth. “Enhanced Pig-to-pig Transmission of a Reassortant H9N2 Influenza Virus Containing 2009 Pandemic H1N1 Internal Genes by Serial Passaging in Pigs.” Third Annual Meeting Belgian Society for Virology. 2015. Print.
APA
Mancera Gracia, J. C., & Van Reeth, K. (2015). Enhanced pig-to-pig transmission of a reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal genes by serial passaging in pigs. Third annual meeting Belgian Society for Virology. Presented at the 3rd Annual meeting of the Belgian Society for Virology.
Chicago author-date
Mancera Gracia, José Carlos, and Kristien Van Reeth. 2015. “Enhanced Pig-to-pig Transmission of a Reassortant H9N2 Influenza Virus Containing 2009 Pandemic H1N1 Internal Genes by Serial Passaging in Pigs.” In Third Annual Meeting Belgian Society for Virology.
Chicago author-date (all authors)
Mancera Gracia, José Carlos, and Kristien Van Reeth. 2015. “Enhanced Pig-to-pig Transmission of a Reassortant H9N2 Influenza Virus Containing 2009 Pandemic H1N1 Internal Genes by Serial Passaging in Pigs.” In Third Annual Meeting Belgian Society for Virology.
Vancouver
1.
Mancera Gracia JC, Van Reeth K. Enhanced pig-to-pig transmission of a reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal genes by serial passaging in pigs. Third annual meeting Belgian Society for Virology. 2015.
IEEE
[1]
J. C. Mancera Gracia and K. Van Reeth, “Enhanced pig-to-pig transmission of a reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal genes by serial passaging in pigs,” in Third annual meeting Belgian Society for Virology, Brussels, Belgium, 2015.
@inproceedings{7197735,
  abstract     = {Avian influenza viruses of H9N2 subtype are endemic in poultry in Asia and the Middle East. Since 1998, they sporadically have caused dead-end infections in humans and swine. Along with avian H7 and H5 influenza viruses, H9N2 is in the top-3 of the world health organization’s list of pandemic influenza virus candidates. On the other hand, the 2009 pandemic H1N1 (pH1N1) virus originated from and has become endemic in swine. Its internal gene cassette has extensively reassorted with established swine influenza viruses all over the world. This pH1N1 internal gene cassette appears to be highly compatible with the surface protein genes of H9N2. This finding has raised concerns about the possible emergence of H9N2 reassortants with public health implications in swine. Moreover, such reassortant viruses showed increased replication and transmissibility in the mouse and ferret model of influenza. The few studies in pigs have also suggested improved fitness of the reassortants as compared to the parental H9N2 virus. We aimed to evaluate if a reassortant H9N2 virus could become better adapted to pigs by serial passaging. To investigate this we performed pig transmission experiments with four different viruses: a reassortant virus containing A/Quail/Hong Kong/G1/97 (H9N2) surface genes and A/California/04/09 (pH1N1) internal genes; another reassortant virus with the same gene constellation that had undergone seven passages in pigs and both parental viruses, H9N2 and pH1N1. Replication efficiency in the porcine lower respiratory tract was minimal for the reassortant H9N2 virus, enhanced for the wholly avian H9N2 virus and greatest for the pig-passaged H9N2 reassortant, with 0, 55 and 93% of the lower respiratory tract samples testing positive for the respective viruses. In pig transmission studies, pH1N1 was excreted in high amounts by all three directly inoculated pigs and six out of six direct contact pigs (mean area under the curve (AUC) for the direct contact pigs of 19,7). In contrast, none of the contact pigs shed high amounts of the parental H9N2 or the original H9N2 reassortant virus (means AUC 3,0 and 4,7, respectively), pointing to inefficient virus transmission. Remarkably, the pig-passaged reassortant was excreted in high titers by four out of six contact animals, with a mean AUC of 16,1. The genetic analysis of the reassortant viruses, to identify which mutations appeared during serial passaging allowing enhanced transmission, is still pending. Our findings confirm that avian H9N2 surface genes are compatible with pH1N1 internal gene cassette, that pigs could serve as suitable intermediate host for the adaptation of reassortant H9N2 virus to mammals, and thus pose a risk of becoming pandemic in humans.},
  articleno    = {abstract 35},
  author       = {Mancera Gracia, José Carlos and Van Reeth, Kristien},
  booktitle    = {Third annual meeting Belgian Society for Virology},
  language     = {eng},
  location     = {Brussels, Belgium},
  title        = {Enhanced pig-to-pig transmission of a reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal genes by serial passaging in pigs},
  url          = {http://www.dmipfmv.ulg.ac.be/vetimmuno/i/Dec18ProgramAbstractBook.pdf},
  year         = {2015},
}