tetano
Editor, Senior Moderator
J Virol. 2015 Mar 11. pii: JVI.00087-15. [Epub ahead of print]
[h=1]Swine PA and NA gene reassortment into human H1N1 is associated with an altered pathogenic phenotype linked to increased MIP-2 expression.[/h] Dlugolenski D[SUP]1[/SUP], Jones L[SUP]1[/SUP], Howerth E[SUP]2[/SUP], Wentworth D[SUP]3[/SUP], Tompkins SM[SUP]1[/SUP], Tripp RA[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Swine are susceptible to infection by both avian and human influenza viruses, and this feature is thought to contribute to novel reassortant influenza viruses. In this study, the influenza virus reassortment rate in swine and human cells was determined. Swine cells co-infected with 2009 pandemic H1N1 (huH1N1), and an endemic swine H1N2 (A/swine/Illinois/02860/09) virus (swH1N2), resulted in a 23% reassortment rate that was independent of alpha 2,3 or 2,6 sialic acid distribution on the cells. The reassortants had altered pathogenic phenotypes linked to introduction of the swine PA and NA into huH1N1. In mice, the huH1N1 PA and NA mediated increased MIP-2 expression early post-infection resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease. The findings support the notion that swine are a mixing vessel for influenza reassortants independent of sialic acid distribution. These results show the potential for continued reassortment of the 2009 pandemic H1N1 virus with endemic swine viruses, and the potential for reassortants to have increased pathogenicity linked to the swine NA and PA genes which are associated with increased pulmonary neutrophil trafficking that is related to MIP-2 expression.
[h=4]IMPORTANCE:[/h] Influenza A viruses can change rapidly via reassortment to create a novel virus, and reassortment can result in possible pandemics. Reassortments among subtypes from avian and human viruses led to the 1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics. Recent analyses of circulating isolates have shown that multiple genes can be recombined from human, avian and swine influenza viruses leading to triple reassortants. Understanding the factors that can affect influenza A virus reassortment is needed for the establishment of disease intervention strategies that may reduce or preclude pandemics. The findings from this study show that swine cells provide a mixing vessel for influenza reassortment independent of differential sialic acid distribution. The findings also establish that circulating NA and PA genes could alter the pathogenic phenotype of the pandemic H1N1 virus resulting in enhanced disease. The identification of such factors provides a framework for pandemic modelling and surveillance.
Copyright ? 2015, American Society for Microbiology. All Rights Reserved.
PMID: 25762737 [PubMed - as supplied by publisher]
[h=1]Swine PA and NA gene reassortment into human H1N1 is associated with an altered pathogenic phenotype linked to increased MIP-2 expression.[/h] Dlugolenski D[SUP]1[/SUP], Jones L[SUP]1[/SUP], Howerth E[SUP]2[/SUP], Wentworth D[SUP]3[/SUP], Tompkins SM[SUP]1[/SUP], Tripp RA[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Swine are susceptible to infection by both avian and human influenza viruses, and this feature is thought to contribute to novel reassortant influenza viruses. In this study, the influenza virus reassortment rate in swine and human cells was determined. Swine cells co-infected with 2009 pandemic H1N1 (huH1N1), and an endemic swine H1N2 (A/swine/Illinois/02860/09) virus (swH1N2), resulted in a 23% reassortment rate that was independent of alpha 2,3 or 2,6 sialic acid distribution on the cells. The reassortants had altered pathogenic phenotypes linked to introduction of the swine PA and NA into huH1N1. In mice, the huH1N1 PA and NA mediated increased MIP-2 expression early post-infection resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease. The findings support the notion that swine are a mixing vessel for influenza reassortants independent of sialic acid distribution. These results show the potential for continued reassortment of the 2009 pandemic H1N1 virus with endemic swine viruses, and the potential for reassortants to have increased pathogenicity linked to the swine NA and PA genes which are associated with increased pulmonary neutrophil trafficking that is related to MIP-2 expression.
[h=4]IMPORTANCE:[/h] Influenza A viruses can change rapidly via reassortment to create a novel virus, and reassortment can result in possible pandemics. Reassortments among subtypes from avian and human viruses led to the 1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics. Recent analyses of circulating isolates have shown that multiple genes can be recombined from human, avian and swine influenza viruses leading to triple reassortants. Understanding the factors that can affect influenza A virus reassortment is needed for the establishment of disease intervention strategies that may reduce or preclude pandemics. The findings from this study show that swine cells provide a mixing vessel for influenza reassortment independent of differential sialic acid distribution. The findings also establish that circulating NA and PA genes could alter the pathogenic phenotype of the pandemic H1N1 virus resulting in enhanced disease. The identification of such factors provides a framework for pandemic modelling and surveillance.
Copyright ? 2015, American Society for Microbiology. All Rights Reserved.
PMID: 25762737 [PubMed - as supplied by publisher]