Sally Furniss
Well-known member
Intersegmental recombination between the haemagglutinin and matrix genes was responsible for the emergence of a highly pathogenic H7N3 avian influenza virus in British Columbia
<nobr>John Pasick<sup>1</sup></nobr>, <nobr>Katherine Handel<sup>1</sup></nobr>, <nobr>John Robinson<sup>2</sup></nobr>, <nobr>John Copps<sup>1</sup></nobr>, <nobr>Deidre Ridd<sup>1</sup></nobr>, <nobr>Kevin Hills<sup>1</sup></nobr>, <nobr>Helen Kehler<sup>1</sup></nobr>, <nobr>Colleen Cottam-Birt<sup>1</sup></nobr>, <nobr>James Neufeld<sup>1</sup></nobr>, <nobr>Yohannes Berhane<sup>1</sup></nobr> and <nobr>Stefanie Czub<sup>1</sup></nobr>
[SIZE=-1] <sup>1</sup> Canadian Food Inspection Agency, National Centre for Foreign Animal Disease, 1015 Arlington Street, Winnipeg, Manitoba, Canada R3E 3M4
<sup>2</sup> Animal Health Centre, British Columbia Ministry of Agriculture and Food, 1767 Angus Campbell Road, Abbotsford, British Columbia, Canada V3G 2M3 [/SIZE]
[SIZE=-1]Correspondence<sup> </sup>
John Pasick<sup> </sup>
jpasick@inspection.gc.ca<script type="text/javascript"><!-- var u = "jpasick", d = "inspection.gc.ca"; document.getElementById("em0").innerHTML = '<a href="mailto:' + u + '@' + d + '">' + u + '@' + d + '<\/a>'//--></script>[/SIZE]
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In February 2004 a highly pathogenic avian influenza (HPAI)<sup> </sup>outbreak erupted in British Columbia. Investigations indicated<sup> </sup>that the responsible HPAI H7N3 virus emerged suddenly from a<sup> </sup>low pathogenic precursor. Analysis of the haemagglutinin (HA)<sup> </sup>genes of the low and high pathogenic viruses isolated from the<sup> </sup>index farm revealed the only difference to be a 21 nt insert<sup> </sup>at the HA cleavage site of the highly pathogenic avian influenza<sup> </sup>virus. It was deduced that this insert most probably arose as<sup> </sup>a result of non-homologous recombination between the HA and<sup> </sup>matrix genes of the same virus. Over the course of the outbreak,<sup> </sup>a total of 37 isolates with, and 3 isolates without inserts<sup> </sup>were characterized. The events described here appear very similar<sup> </sup>to those which occurred in Chile in 2002 where the virulence<sup> </sup>shift of another H7N3 virus was attributed to non-homologous<sup> </sup>recombination between the HA and nucleoprotein genes.<sup> </sup>
<!-- null --> Supplementary material of the gross and microscopic lesions<sup> </sup>produced in experimentally infected chickens can be found in<sup> </sup>JGV Online.
http://vir.sgmjournals.org/cgi/content/full/86/3/727?ck=nck
<nobr>John Pasick<sup>1</sup></nobr>, <nobr>Katherine Handel<sup>1</sup></nobr>, <nobr>John Robinson<sup>2</sup></nobr>, <nobr>John Copps<sup>1</sup></nobr>, <nobr>Deidre Ridd<sup>1</sup></nobr>, <nobr>Kevin Hills<sup>1</sup></nobr>, <nobr>Helen Kehler<sup>1</sup></nobr>, <nobr>Colleen Cottam-Birt<sup>1</sup></nobr>, <nobr>James Neufeld<sup>1</sup></nobr>, <nobr>Yohannes Berhane<sup>1</sup></nobr> and <nobr>Stefanie Czub<sup>1</sup></nobr>
[SIZE=-1] <sup>1</sup> Canadian Food Inspection Agency, National Centre for Foreign Animal Disease, 1015 Arlington Street, Winnipeg, Manitoba, Canada R3E 3M4
<sup>2</sup> Animal Health Centre, British Columbia Ministry of Agriculture and Food, 1767 Angus Campbell Road, Abbotsford, British Columbia, Canada V3G 2M3 [/SIZE]
[SIZE=-1]Correspondence<sup> </sup>
John Pasick<sup> </sup>
jpasick@inspection.gc.ca<script type="text/javascript"><!-- var u = "jpasick", d = "inspection.gc.ca"; document.getElementById("em0").innerHTML = '<a href="mailto:' + u + '@' + d + '">' + u + '@' + d + '<\/a>'//--></script>[/SIZE]
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<table bgcolor="#e1e1e1" cellpadding="0" cellspacing="0" width="100%"> <tbody><tr><td align="left" bgcolor="#ffffff" valign="middle" width="5%">
[/SIZE]</th></tr></tbody></table>
In February 2004 a highly pathogenic avian influenza (HPAI)<sup> </sup>outbreak erupted in British Columbia. Investigations indicated<sup> </sup>that the responsible HPAI H7N3 virus emerged suddenly from a<sup> </sup>low pathogenic precursor. Analysis of the haemagglutinin (HA)<sup> </sup>genes of the low and high pathogenic viruses isolated from the<sup> </sup>index farm revealed the only difference to be a 21 nt insert<sup> </sup>at the HA cleavage site of the highly pathogenic avian influenza<sup> </sup>virus. It was deduced that this insert most probably arose as<sup> </sup>a result of non-homologous recombination between the HA and<sup> </sup>matrix genes of the same virus. Over the course of the outbreak,<sup> </sup>a total of 37 isolates with, and 3 isolates without inserts<sup> </sup>were characterized. The events described here appear very similar<sup> </sup>to those which occurred in Chile in 2002 where the virulence<sup> </sup>shift of another H7N3 virus was attributed to non-homologous<sup> </sup>recombination between the HA and nucleoprotein genes.<sup> </sup>
<!-- null --> Supplementary material of the gross and microscopic lesions<sup> </sup>produced in experimentally infected chickens can be found in<sup> </sup>JGV Online.
http://vir.sgmjournals.org/cgi/content/full/86/3/727?ck=nck