Thanks for the experiment! Given that shares were worked down all day, I was bitching to Schwab at the same time that I was praising them for saving me bucks.
;-)
I was going to park this in the SARS/b.f. thread, but since I'm already replying your post....... just parking.....
J Virol. 2007 Jun 6; [Epub ahead of print] Molecular changes in the polymerase genes (PA and PB1) associated with high pathogenicity of H5N1 influenza virus in Mallard ducks.
Hulse-Post DJ, Franks J, Boyd K, Salomon R, Hoffmann E, Yen HL, Webby RJ, Walker D, Nguyen TD, Webster RG.
St. Jude Children's Research Hospital, Department of Infectious Diseases, Division of Virology, Memphis, TN; St. Jude Children's Research Hospital, Animal Resources Center, Memphis, TN; Department of Virology, National Institute of Veterinary Research, Ministry of Agriculture and Rural Development, Hanoi, Vietnam.
Highly pathogenic (HP) H5 and H7 influenza viruses are usually non-pathogenic in mallard ducks. However, the currently circulating HP H5N1 viruses acquired a different phenotype and are able to cause mortality in Mallards. To establish the molecular basis of this phenotype, we cloned the human A/Vietnam/1203/04 (H5N1) influenza virus isolate that is HP in ferrets, mice, and mallards and found it to be a heterogeneous mixture. Large-plaque isolates were highly pathogenic to ducks, mice, and ferrets, whereas the small-plaque isolates were non-pathogenic in these species. Sequence analysis of the entire genome revealed that the small-plaque and large-plaque isolates differed in the coding of 5 amino acids. There were two differences in the hemagglutinin (HA) gene (K52T; A544V), one in the PA gene (T515A), and two in the PB1 gene (K207R; Y436H). We inserted the amino acid changes into the wild-type reverse-genetic virus construct to assess their effect on pathogenicity in vivo. The HA mutations and the PB1 K207R mutation did not alter the HP phenotype of the large-plaque virus, whereas constructs with the PA (T515A) and PB1 (Y436H) mutations were nonpathogenic in orally inoculated ducks. The PB1 (Y436H) construct was not efficiently transmitted in ducks, whereas the PA (T515A) construct replicated as well as the wild-type virus and was transmitted efficiently. These results show that the PA and PB1 genes of HP H5N1 influenza viruses are associated with lethality in ducks. The mechanisms of lethality and the perpetuation of this lethal phenotype in ducks in nature remain to be determined. |