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trH1N2 Minnesota Mutation
The above comments are on the recently reported trH1N2 case (1M) in Minnesota, A/Minnesota/19/2011, which is being compared to the 2007 trH1N2 cases in Michigan, because that is the only confirmed human H1N2 triple reassortant.
However, the 2011 case in Minnesota is related to the 2010 human trH3N2 cases (A/Pennsylvania/40/2010 and A/Wisconsin/12/2011) and contains PB1 E618D, which was in all six reported human 2010 trH3N2 cases. These sequences reasserted with a swine trH1N2 similar to the recently released sequences from Ohio, A/swine/Ohio/FAH10-1/2010, which contributed PB1, NA, and MP, which swapped out the PB1 with H1N1pdm09 E618D acquired by recombination, but added the H1N1pdm09 M gene, as well as the N2 in multiple swine H1N2, as well as the other 2010 Pennsylvania isolate, A/Pennsylvania/14/2010.
The creation of the trH1N2 in Minnesota involved the same parental sequences, but the acquisition was limited to the H1 and N2 surface genes Thus, the Minnesota 2011 isolate has a novel H1 and N2 combination on the outside, but the human trH3N2 genes on the inside, including PB1 with E618D.
Therefore, this novel human H1N2 is another example of a case with H1N1pdm09 PB1 E618D (which was present in all six 2010 isolates), or H1N1pdm09 M gene, which is in all 11 other trH3N2 2011 isolates.
These novel reassortants raise serious concerns because there now are 18 examples identified in 2010 and 2011, all of which have a link to H1N1pdm09, and the five most recent cases have no linkage to “swine exposure”, indicating three different triple reassortants (H3N2pdm11, trH3N2, trH1N2) are co-circulating in the human population raising serious and complex pandemic concerns.