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Commentary

Hong Kong Swine trH3N2 Distinct From US Human Isolates
Recombinomics Commentary 13:40
November 17, 2011

Flu expert Malik Peiris said the H3N2 subtype seen in the pigs is not the same swine-originated new H3N2 that has infected seven people in the United States since July.

The above comments note that the 15 trH3N2 Hong Kong swine isolates from August to October collections from the Sheung Shui Slaughterhouse in Hong Kong were distinct from the 2011 trH3N2 isolates from patients in Indiana, Pennsylvania, and Maine.  The recent Hong Kong isolates are similar to 16 trH3N2 isolates from collections from May to July from the same slaughterhouse.  These isolates were identified fro enhanced swine surveillance in Hong Kong, where there are SOIV’s similar to those in the United States.

The 2009 pandemic spread H1N1pdm09 worldwide in humans, which then led to the jump back into swine worldwide, including Hong Kong and China, which led to further reassortment which created SOIV’s with H1N1pmd09 genes, including trH3N2 like those described above.
However, the human trH3N2 cases in the United States were first reported in 2009, and many of the internal genes linked back to a trH1N1 outbreak at a fair in Huron, Ohio in 2007.  Two human cases were identified (A/Ohio/01/2007 and A/Ohio/02/2007), but 2 dozen attendees had flu-like symptoms, which is uncommon in August in Ohio, suggesting many were infected with the same virus, which was also isolated from swine at the fair.  In late 2010 human trH3N2 sequences clustered, including two isolates, A/Pennsylvania/40/2010 and A/Wisconsin/12/2010, which matched each other in all 8 gene segments.  Human to human transmission was lab confirmed in a cluster from Minnesota, and the isolate from the index case, A/Minnesota/11/2011, was related to most of the genes in the PA and WI isolates, and Minnesota/11 was selected as the target for a trH3N2 pandemic vaccine.

In 2011 a novel trH3N2 was identified which evolved from the 2010 human isolates.  5 of the genes matched the genes in the dominant human trH3N2 sequences, including H3 (PB2, PA, HA, NP, NS).  The PB1 was an earlier version which was similar to the Ohio sequences from 2007 and the NA matched A/Pennsylvania/14/2010, from one of the cases in the WHO pager alert (the H3 matched the other cases in the alert).  In addition to the genes matching the earlier human trH3N2 cases, the novel virus in 2011 also had an M gene from H1N1pdm.  All seven human trH3N2 cases from 2011 have the same constellation of genes, with the same lineages described above.

This constellation of 7 trH3N2 genes and an M gene from H1N1pdm09 has not been reported in any swine.  The 31 recent trH3N2 isolates from Hong Kong have multiple H1N1pdm genes, and the trH3N2 genes are from lineages that do not match the human isolates.

Similarly, enhanced surveillance in the US which include 26 triple reassortants from 2011 also fail to match the human isolates, although many match the lineages for some of the genes, including the H3 and N2 combination or the N2 / M gene combination, but none match all eight gene segments.
 
Thus, in the US and Hong Kong there have been more than 50 swine triple reassortants from 2011 identified and none match the human isolates, while all 7 of the 2011 human isolates have the same constellation and a match for all 8 gene segments, signaling human transmission.

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