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Commentary
Media Myths on
trH3N2 Evolution and Significance
Recombinomics Commentary 20:20
November 25, 2011
"I don't think this is anything to worry about for the moment," Monto says. "We have known that swine viruses get into humans occasionally, transmit for a generation or two and then stop. The issue is whether there will be sustained transmission (from person to person)- and that nearly never happens."
The above comments ignore the evolution of the novel trH3N2 and the appearance of the same constellation and lineage in all ten 2011 cases, which involved two independent outbreaks in Indiana, two in Maine, and large clusters in Pennsylvania and Iowa. Moreover, the 2011 novel trH3N2 evolved from the 2010 human trH3N2 sequences which were clearly clustering.
The comments above are in a time warp that ended in 2009. Prior to the 2009 H1N1 pandemic, there were thirteen human cases involving H1 triple reassortants, which behaved as described above. A year ago the CDC released full sets of sequences from these cases, and more sequences from swine were released due to increased surveillance. The human sequences were scatter among the swine sequences, demonstrating jumps of virus from swine to humans that did not expand.
However, after the start of the 2009 H1N1 pandemic, the first trH3N2 cases in humans in the United States were reported. A year ago it became clear that the sequences from isolates in the 2010 cases began to cluster and branches that had a limited number of swine isolates, signaling adaptation to humans. two of the isolates, A/Wisconsin/12/2011 and A/Pennsylvania/40/2011, were virtually identical to each other even though the cases were nit epidemiologically linked. These two cases were then followed by a cluster in Minnesota. A/Minnesota/11/2010 was isolated from the index case, and his daughter, who had no contact with swine, was lab confirmed (serologically) trH3N2. Moreover, most of the gene matched the isolates from Wisconsin and Pennsylvania.
The matching took a dramatic turn in 2011. The first sequence had evolved from the human 2010 trH3N2 isolates, but had acquired the M gene from H1N1pdm, and the NA gene from another human isolate from 2010. This novel constellation was then matched by all three cases in Pennsylvania, which was then matched by the subsequent cases in Indiana, Maine, and Iowa.
Thus, the history of the H1 triple reassortants has little bearing on the novel human contagion that has emerged in 2011. The latest examples involve five cases in Iowa. trH3N2 was isolated from three, but the father and brother of the index case developed symptoms shortly before or after the index case, leaving little doubt that all five cases were infected with the same novel trH3N2 via human to human transmission.
The absence of any swine exposure destroys the CDC narrative on swine exposure, and the number of cases will explode as testing increases, ancient history lessons on H1 triple reassortants, notwithstanding.
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