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Commentary

H1N1pdm09 M Gene Drives Genetic Instability In American Swine
Recombinomics Commentary 12:45
December 06, 2011

The emergence of trH3N2 with an H1N1pdm09 M gene (H3N2pdm11) has focused attention on two recent papers discussing the impact of the acquisition of H1N1pdm09.  One report noted that H1N1pdm M was critical for the efficient transmission of H1N1pdm in humans using a guinea pig model.  The other report noted that the jump of H1N1pdm09 into North American swine was association with an increase in the frequency of reassortment, with all of the reassortants containing the M gene and at least two additional H1N1pdm09 genes.

Most of the examples cited were H1N2, but one of the examples was a 2009 trH3N2 isolate, A/swine/Minnesota/239105/2009, which had acquired three H1N1pdm09 genes (PA, NP, MP).  However, further analysis indicated the trH3N2 precursor for this isolate was also the precursor for the two 2010 trH3N2 isolates from Iowa
(A/swine/Iowa/A01049034/2010, and A/swine/Iowa/A01049035/2010), which matched the constellation of H3N2pdm11, which had 7 trH3N2 genes plus 1 H1N1pdm09 gene.  Moreover, the two isolates from Iowa , had also acquired a H3N2pdm11 NP gene.  Thus, the precursor for the two Iowa isolates had one gene (NP) acquired from H3N2pdm11 and another gene (MP) from H1N1pdm09.

This increased activity in reassortment was also present in the recently released sequences from Kansas.  The sequences from Kansas were full sequences, which indicated this series had three genes from H1N1pdm09 (NP, MP, NS), but one isolate, A/swine/Kansas/11-107824/2011) also has PB2 and PA from H1N1pdm09, signaling the third trH3N2 constellation based on H1N1pdm09 acquisitions, and like the H1N2 isolates in the above publication, all contain an M gene from H1N1pdm09.

The number of trH3N2 isolates with H1N1pdm09 also continues to increase, although most of the recent sequences only include data for H1, N2, and MP.  These isolates have an N2 that is closely related to the N2 in H3N2pdm11, while the H1 is from seasonal H1 circulating in 2003.
Thus, the release of H3N2 and H1N2 sequences with H1N1pdm09 M gene continues to dramatically increase the number of triple reassortants with an H1N1pdm09 M gene, yet only one swine isolate,
A/swine/NY/A01104005/2011, has the H3N2pdm11 sub-clade, signaling transmission of this sub-clade in humans.

Moreover, there is also increased reassortment within sub-clades, such as the NP identity between A/swine/Kansas/11-110529/2011 and A/swine/Kansas/11-107824/2011.  This type of increased reassortment within the H3N2pdm11 sub-clade, which also supports the transmission of H3N2pdm11 in humans.

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