H3N2v Sequences Refute CDC Swine Exposure Message



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H1N1 Consulting Paradigm Shift Viral Evolution Intervention Monitoring Vaccine Screening Vaccine Development Expression Profiling Drug Discovery Custom Therapies Patents	Audio:Aug8 Aug16 Aug31 Sep6 twitter Commentary H3N2v Sequences Refute CDC Swine Exposure Message Recombinomics Commentary 15:00 September 6, 2012 Found in U.S. pigs in 2010 and humans in July 2011, this H3N2v virus appears to spread more easily from pigs to people than other variant influenza viruses. Most reported cases to date have occurred in people who are exhibiting or helping to exhibit pigs at fairs this season after close and prolonged contact with pigs. "So far more than 90 percent of cases have occurred in people who are exhibiting or helping to exhibit pigs, or who are family members of these people. That is why our message is so targeted," says Finelli. The above comments are from the August 31 CDC update on H3N2v and the comment that “this H3N2v virus” appearing first in humans in July 2011 clearly refers to the sub-clade represented by A/Indiana/08/2011, which has an H1N1pdm09 M gene. However, the claim that this sub-clade was found in pigs in 2010 is not supported by any public data, and is unlikely to be supported by any private data. Although the presence of the H1N1pdm09 M gene in H3N2 was found in swine in 2010, those isolates were easily distinguished from the 2011 sub-clade and have never been reported in human cases. Moreover, the initial human H3N2v cases in 2011 were formed via reassortment between the dominant human H3N2v sub-clade in 2010 (which did not have an H1N1pdm09 M and contributed 5 gene segments (PB2, PA, HA, NP, NS) and swine H1N2, which contributed PB1, NA and an H1N1pdm09 M gene. A recently published peer reviewed (Journal of Virology) paper entitled “The evolution of novel reassortant A/H3N2 influenza viruses in North American swine and humans, 2009–2011” described public and newly released swine sequences and found one match, A/swine/NY/A01104005/2011, which was from a sample collected September 13, 2011. The USDA subsequently released additional sequences which increased the number of matches (based on a minimal requirement of HA, NA, and MP matches for the lineage of the human cases in 2011) to 26, which included three isolates (A/swine/Iowa/A01202529/2011, A/swine/Iowa/A01202530/2011, A/swine/Iowa/A01202573/2011) from samples collected prior to the New York isolate. However, the earliest collection date is August 22, 2011, which is well after 2010 and after the first human cases in July, 2011. Moreover, the sub-clade linked to the human H3N2v cases changed in late 2011 when H3N2v was isolated from children at a Mineral County day care center (A/West Virginia/06/2011 and A/West Virginia/07/2011) when had a NA gene with a lineage found in H3N2 swine. This novel sub-clade has been found in all human 2012 cases, but only found in 2 (A/swine/North Carolina/A01203272/2012 and A/swine/Indiana/A01203509/2012) of the 26 matches. Yesterday, the USDA released sequences from the first swine isolate, A/swine/Indiana/A00968380/2012, from the explosion pf human H3N2v cases in July and August. However, this LaPorte swine isolate did not match the four human H3N2v sequences from the LaPorte outbreak. Moreover, of the 24 swine isolates that match the initial 2011 cases, including 17 isolates from 2012 collections, none match a reported human 2012 sequence. Thus, although the CDC continues to cite swine exposure as a cause for the 2012 human H3N2v cases, this position is not supported by sequence data, and is dependent on heavily biased testing of cases with swine exposure. Media Link Recombinomics Presentations Recombinomics Publications Recombinomics Paper at Nature Precedings

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