tetano
Editor, Senior Moderator
J Gen Virol. 2016 Dec 9. doi: 10.1099/jgv.0.000678. [Epub ahead of print]
[h=1]A highly pathogenic avian influenza virus H5N1 with 2009 pandemic H1N1 internal genes demonstrates increased replication and transmission in pigs.[/h] Abente EJ[SUP]1[/SUP], Kitikoon P[SUP]2[/SUP], Lager KM[SUP]3[/SUP], Gauger PC[SUP]4[/SUP], Anderson TK[SUP]5[/SUP], Vincent A[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] This study investigated the pathogenicity and transmissibility of a reverse-genetics derived highly pathogenic avian influenza (HPAI) H5N1 lineage influenza A virus (IAV) that was isolated from a human, A/Iraq/755/06. We also examined surface gene reassortant viruses comprised of the HA and NA from A/Iraq/755/06 and the internal genes of a 2009 pandemic H1N1 virus, A/New York/18/2009 (2Iraq/06:6NY/09 H5N1), and HA and NA from A/New York/18/2009 with the internal genes of A/Iraq/755/06 (2NY/09:6Iraq/06 H1N1). The parental A/Iraq/755/06 caused little to no lesions in swine, limited virus replication was observed in the upper respiratory and lower respiratory tract, and transmission was detected in 3/5 direct contact pigs based on seroconversion, detection of viral RNA, or virus isolation. In contrast, the 2Iraq/06:6NY/09 H5N1 reassortant caused mild lung lesions, demonstrated sustained virus replication in the upper and lower respiratory tracts, and transmitted to all contacts (5/5). The 2NY/09:6Iraq/06 H1N1 reassortant also caused mild lung lesions, there was evidence of virus replication in the upper respiratory and lower respiratory tract, and transmission was detected in all contacts (5/5). These studies indicate that a HPAI-derived H5N1 reassortant with pandemic internal genes may be more successful in sustaining infection in swine, and that HPAI-derived internal genes were marginally compatible with pandemic 2009 H1N1 surface genes. Comprehensive surveillance in swine is critical to identify a possible emerging HPAI reassortant in all regions with HPAI in wild birds and poultry and H1N1pdm09 in pigs or other susceptible hosts.
PMID: 27959778 DOI: 10.1099/jgv.0.000678
[PubMed - as supplied by publisher]
[h=1]A highly pathogenic avian influenza virus H5N1 with 2009 pandemic H1N1 internal genes demonstrates increased replication and transmission in pigs.[/h] Abente EJ[SUP]1[/SUP], Kitikoon P[SUP]2[/SUP], Lager KM[SUP]3[/SUP], Gauger PC[SUP]4[/SUP], Anderson TK[SUP]5[/SUP], Vincent A[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] This study investigated the pathogenicity and transmissibility of a reverse-genetics derived highly pathogenic avian influenza (HPAI) H5N1 lineage influenza A virus (IAV) that was isolated from a human, A/Iraq/755/06. We also examined surface gene reassortant viruses comprised of the HA and NA from A/Iraq/755/06 and the internal genes of a 2009 pandemic H1N1 virus, A/New York/18/2009 (2Iraq/06:6NY/09 H5N1), and HA and NA from A/New York/18/2009 with the internal genes of A/Iraq/755/06 (2NY/09:6Iraq/06 H1N1). The parental A/Iraq/755/06 caused little to no lesions in swine, limited virus replication was observed in the upper respiratory and lower respiratory tract, and transmission was detected in 3/5 direct contact pigs based on seroconversion, detection of viral RNA, or virus isolation. In contrast, the 2Iraq/06:6NY/09 H5N1 reassortant caused mild lung lesions, demonstrated sustained virus replication in the upper and lower respiratory tracts, and transmitted to all contacts (5/5). The 2NY/09:6Iraq/06 H1N1 reassortant also caused mild lung lesions, there was evidence of virus replication in the upper respiratory and lower respiratory tract, and transmission was detected in all contacts (5/5). These studies indicate that a HPAI-derived H5N1 reassortant with pandemic internal genes may be more successful in sustaining infection in swine, and that HPAI-derived internal genes were marginally compatible with pandemic 2009 H1N1 surface genes. Comprehensive surveillance in swine is critical to identify a possible emerging HPAI reassortant in all regions with HPAI in wild birds and poultry and H1N1pdm09 in pigs or other susceptible hosts.
PMID: 27959778 DOI: 10.1099/jgv.0.000678
[PubMed - as supplied by publisher]