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Fuzzy CDC Summary of SOIV /  trH3N2 In Humans Needs Update
Recombinomics Commentary 09:00
October 22, 2011

As of October 14, 2011, 26 cases of human infection with swine origin influenza viruses have been reported in the United States. These are viruses that normally infect pigs. Like human influenza viruses, there are different subtypes and strains of swine-origin influenza viruses. The main swine influenza viruses circulating in U.S. pigs in recent years are swine triple reassortant (tr) H1N1 influenza virus, trH3N2 virus and trH1N2 virus. Of the 26 human cases reported since 2005, 12 have been trH1N1 viruses, 13 have been trH3N2 viruses and one has been a trH1N2 virus. All 26 persons infected with swine viruses recovered from their illness. Nineteen cases occurred in children (persons 18 or younger) and 7 cases occurred in adults. In 22 cases, direct or indirect exposure to swine prior to onset of illness has been identified. Likely transmission of swine-origin influenza virus from close contact with an infected person has been observed in investigations of human infections with swine-origin influenza A virus, but has not resulted in sustained human-to-human transmission.

The above paragraph summarizes swine originating influenza virus (SOIV) in humans in the United States since 2005, and it has been updated to include the most recent case (8M) from Maine.  Although the CDC SOIV site includes titles and links to individual CDC reports, including MMWR summaries/reports and “have you heard” reports which include coverage of the five cases in 2011, the above summary fails to capture the dramatic shift in these cases since the 2009 H1N1 pandemic. 

All of the 13 H1 triple reassortants (12 trH1N1 and 1 trH1N2) have been identified prior to the H1N1 pandemic and all 13 of the H3 triple reassortants (trH3N2) have been identified after the start of the 2009 pandemic.  Moreover, all of the 2011 trH3N2 have the M gene from pandemic H1N1 (H1N1pdm09) and have the same set of gene segments linked to earlier tr human cases (PB2, PA, HA, NP, NS from dominant 2010 human trH3N2 cases, A/Pennsylvania/40, 2010, A/Wisconsin/12/2010, A/Minnesota/11/2010; PB1 from 2007 H1N1 cluster in Ohio, A/Ohio/01/2007 and A/Ohio/02/2007; and NA from first reported trH3N2 case in Pennsylvania, A/Pennsylvania/14/2010.

The shift from trH1N1 to trH3N2 reported cases may be due in part to testing, since trH1N1 have an H1 related to H1N1pdm09 and current H1 sub-typing either would not distinguish between the two lineages or would be negative for trH1N1, limiting detection. 

However, the detection of trH3N2 reflects are true increase in frequency of this serotype in humans in the United States.  This increase is likely linked to the acquisition of PB1 E618D, which is present in virtually all H1N1pdm09 isolates, which is also in 6 of the 7 public PB1 sequences from cases detected prior to 2011.  This gene has been replaced by gene segment more closely related to Ohio trH1N1 sequences and E618D may play a lesser role since the 2011 isolates have also acquired the M gene from H1N1pdm09, which is critical for human to human transmission.

Thus, the updated summary table on SOIV in humans in the US since 2005 should reflect the dramatic shift from trH1 to trH3 cases, as well as the emergence of trH3N2 with the H1N1pdm09 M gene segment in 2011.

Similarly the statement on human to human (H2H) transmission should indicate that the absence of  H2H is based on epidemiological studies, which is strongly refuted by the sequence data linking the human 2011 trH3N2 cases to most of the gene segments in the human 2010 trH3N2 cases and the absence of this constellation in swine.

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