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Media Myth On
Relatedness Between Novel H1N2 and H3N2
The above comments from a Helen Branswell piece on the two new human cases involving variations of H3N2pdm11 suggests that the origin of the trH1N2 case (A/Minnesota/19/2011, may have been identified, which if confirmed would represent another cluster and more direct evidence for human transmission.
However, the above comment also spreads the media myth that the trH1N2 case is unrelated to the latest trH3N2 case (A/West Virginia/06/2011) and the earlier 10 cases, designated H3N2pdm11. These viruses have evolved from the 2010 human cases, and consequently share 7 of 8 genes with these cases. The latest human cases signal extreme instability, which has been noted in the recent swine cases, but now is appearing in the human cases also.
The recently release sequences from the Ohio swine, A/swine/Ohio/FAH10-1/2010, had the missing pieces of the puzzle for the creation of H3N2pdm11, which had five gene segments from the dominant 2010 trH3N2 cases (PB2, PA, HA, NP, NS) and three gene segments from the H1N2 Ohio swine (PB1, NA, MP). These donor sequences are widespread in swine which led to a co-infection and the creation of the H3N2pdm11 reassortant.
The first 10 human cases in 2011 had evidence of reassortment within the sub-clade, but the latest cases has evidence for additional reassortment with sequences outside of the H3N2pdm11 sub-clade. The trH3N2 case (A/West Virginia/06/2011) has an NA gene from swine triple reassortants (present in trH3N2 and trH1N2), while the trH1N2 has swapped out the H3 for an H1 leading to the new serotype. However, the remaining 7 genes match the trH3N2 genes or the 2010 human trH3N2 precursor genes.
Thus, the virus is very unstable, but spreading in humans, and most easily detected in children under 10, which account of 11 of 12 cases in 2011.
Thus, both cases reported today are closely related to the trH3N2 in the prior 10 cases, but have reassorted to change one of the eight gene segments to one most commonly found in swine prior to 2011.
The lack of a serious surveillance program targeting those under 10, and a fixation on “swine exposure” and requests for such samples, has created an illusion that the 2011 H3N2 cases are due to limited transmission, which really is due to limited testing of the most vulnerable population.