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Commentary

ProMED Comments on Swine Exposure By trH3N2 Cases
Recombinomics Commentary 18:30
October 21, 2011

The Maine virus is genetically similar to 4 previous cases identified in the United States this year (2011), 3 in Pennsylvania, and one in Indiana (see the ProMED-mail references below), all of which had exposure to swine. - Mod.CP]

All four children were infected with swine-origin influenza A (H3N2) viruses; two were hospitalized; all four have since recovered from their illness. The case in Indiana did not report exposure to pigs prior to illness onset, although an epidemiologic investigation concluded human to human transmission was likely as a close contact reported direct contact with pigs prior to the child’s illness onset.

The above comments are from the ProMED report on the recent case (8M) of trH3N2 infection in Cumberland County, Maine, and the week 40 FluView describing the four prior 2011 cases with an M gene from pandemic H1N1, which clearly state that the Indian case (2M) did not have a swine exposure, which was also stated in the original early release MMWR, which like the FluView report, concluded that the Indiana case was due to limited human to human transmission.

The ProMED report was from the advisory issued by the Maine CDC, but ProMED usually edits reports and provides clarity, which was not done in this case.  Instead ProMED, which has a wide readership including media reporters, perpetuated the myth that the trH3N2 cases were infected by swine, which has rarely been demonstrated in trH3N2 cases and has not been demonstrated in any of the 2011 cases, including the case from Maine.  The Maine and three Pennsylvania cases attended agricultural fairs where swine was exhibited, but there have been no reports of influenza symptoms in the swine and no SOIV has been isolated.  Moreover, all 5 human cases in 2011 have the same constellation of genes, including an M gene from H1N1, and this constellation has not been reported in any swine, including 2011 isolates in the United States identified by aggressive surveillance programs by the USDA and academic institutions.

Moreover, the sequences from the Maine isolate, A/Maine/06/2011, have several genes which began evolving from closely related sequences in human 2010 trH3N2 sequences, indicating this common constellation for all five human 2011 cases began diverging prior to July, 2011, which overlaps the time frame for US 2011 swine isolates, supporting evolution in humans rather than swine.

ProMED should correct the quote in the above report, which states that all 2011 trH3N2 case had swine exposure, when the Indiana case has no such exposure, as indicated in the CDC’s FluView and MMWR.

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