ABSTRACT
Reassortant influenza viruses with combinations of avian, human and/or swine genomic segments have been frequently detected in pigs. As a consequence, pigs have been accused of being a “mixing vessel” for influenza viruses.This implies that pig cells support transcription and replication of avian influenza viruses in contrast to human cells in which most avian influenza virus polymerases display limited activity.
Although influenza polymerase activity has been studied in human and avian cells for many years using a minigenome assay, similar investigation in pig cells has not been reported. We developed the first minigenome assay in pig cells and compared activities of avian or human influenza-origin polymerases in pig, human and avian cells. We also investigated in pig cells the consequences of some known mammalian host range determinants that enhance influenza polymerase activity in human cells such as PB2 mutations E627K, D701N, G590S/Q591R and T271A. The two typical avian influenza virus polymerases used in this study were poorly active in pig cells, similar to what is seen in human cells and mutations that adapt the avian influenza polymerase for human cells also increased activity in pig cells. In contrast, a different pattern was observed in avian cells. Finally, highly pathogenic avian influenza H5N1 polymerase activity was tested because this subtype has been reported to replicate only poorly in pigs. H5N1 polymerase was active in swine cells, suggesting that other barriers restrict these viruses from becoming endemic in pigs.
[editing is mine]
http://jvi.asm.org/content/early/2012/10/11/JVI.01633-12.abstract
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