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Commentary Week 42 MMWR
Reports Seventh trH3N2 Case In 2011 The above comments from the week 42 MMWR confirm that the novel influenza listed in the provisional table was trH3N2, and is almost certainly the last reported case (8M) from Maine, A/Maine/06/2011. The seven cases confirmed in 2011 strongly support human to human (H2H) and contradict the CDC narrative citing a very loose “swine exposure” as a source of the infections. The first case confirmed in 2011 is from a 2010 infection in a case, A/Pennsylvania/40/2010. who was symptomatic on Sept 6, 2010, a week prior to the Wisconsin case, A/Wisconsin/12/2010, and 7 weeks prior to Pennsylvania case, A/Pennsylvania/14/2010, which were the subject of the WHO pager alert. That alert noted the Wisconsin and Pennsylvania cases and assurance were then issued by the CDC that the two cases had sequence differences indicating that the infectiones were not from a common source. However, the sequence from the first Pennsylvania case was virtually identical to the Wisconsin case, but the reporting of the first Pennsylvania case delayed 5 months due to technical issues linked to the growth and isolation of the virus. However, the CDC has a PCR tested for swine H3, which can quickly identify trH3N2 in samples directly. Similarly, the CDC can sequence from the clinical sample without virus isolation. These abilities were clearly demonstrated in the Maine case. The state agency notified the CDC of an influenza A positive, subtype inconclusive case, on October 14. The CDC confirmed trH3N2 on October 16, and released full sequences for all eight gene segments on October 17, using the clinical sample collected in Maine on October 10. Thus, cases that support the CDC can be analyzed and reported in a few days, not 5 months. A long delay was also associated with the second trH3N2 reported in 2011. This was another 2010 case who was the daughter of a case (31M) confirmed in 2010, A/Minnesota/11/2010. She had no swine contact and her trH3N2 was confirmed serologically. Other symptomatic family members were “inconclusive” for trH3N2, suggesting many family members were infected by A/Minnesota/11/2010, and the CDC has used this isolate to create an H3N2 pandemic vaccine. This cluster represented the first acknowledged H2H transmission of trH3N2. However, the five trH3N2 cases infected in 2011 provide compelling evidence that this new human contagion is widespread in humans. In 2010 most of the human cases shared most of the flu trH3N2 genes, but in 2011 this clustering evolved into identities where all 5 2011 cases match each other in all five gene segments, including an M gene from H1N1pdm09, which was critical for the jump of H1N1 from swine to humans. The first 2011 case, A/Indiana/08/2011, had no swine contact. His caretaker had swine exposure, but the caretaker and swine were asymptomatic and no SOIV has been reported. Moreover, enhanced surveillance of swine in the United States and swine worldwide has failed to identify the constellation present in all five human cases. Moreover, the next three cases attended the Washington County Fair in Pennsylvania and two of the sequences, A/Pennsylvanai/10/2011 and A/Pennsylvania/11/2011, were virtually identical to the Indiana, infected a month earlier, while the third case in Pennsylvania, A/Pennsylvania/09/2011, was a drift variant, signaling a second source for the Pennsylvania, but the constellation of gene segments was the same. The most recent case from Maine, A/Maine/06/2011, is also a drift variant. It began to diverge from the 2010 sequences at an earlier date, adding support for a widespread distribution of this human contagion. However, all five of the confirmed 2011 trH3N2 have a loose association with swine exposure raising concerns that case with no swine exposure have not been disclosed because they are still being investigated for a swine exposure, leading to bizarre reporting of unsubtypables, which resemble a shell game, with clear examples of “now you see it / now you don’t”. Recombinomics
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