Abstract:
:Despite reports that the PB1-F2 protein contributes to influenza virus pathogenicity in the mouse model, little is known about its significance in avian hosts. In our previous study, the A/Vietnam/1203/04 (H5N1) wild-type virus (wtVN1203) was more lethal to mallard ducks than a reverse genetics (rg)-derived VN1203. In search of potential viral factors responsible for this discrepancy, we found that synonymous mutations (SMs) had been inadvertently introduced into three genes of the rgVN1203 (rgVN1203/SM-3). Of 11 SMs in the PB1 gene, three resided in the PB1-F2 open reading frame, caused amino acid (aa) substitutions in the PB1-F2 protein, and reduced virus lethality in mallard ducks. The wtVN1203 and recombinant viruses with repairs to these three aa's (rgVN1203/R-PB1-F2) or with repairs to all 11 SMs (rgVN1203/R-PB1) were significantly more pathogenic than rgVN1203/SM-3. In cultured cells, repairing three mutations in PB1-F2 increased viral polymerase activity and expression levels of viral RNA.
journal_name
Arch Viroljournal_title
Archives of virologyauthors
Marjuki H,Scholtissek C,Franks J,Negovetich NJ,Aldridge JR,Salomon R,Finkelstein D,Webster RGdoi
10.1007/s00705-010-0666-4subject
Has Abstractpub_date
2010-06-01 00:00:00pages
925-34issue
6eissn
0304-8608issn
1432-8798journal_volume
155pub_type
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