Paradigm Shift Intervention Monitoring
twitter
Commentary
CDC H3N2pdm11
Name Blame Game
Recombinomics Commentary 23:45
December 02, 2011
This H3N2 poses similar naming challenges. There is already a human H3N2 — a distant cousin of this pig virus — so some way to differentiate the viruses is needed. Pork producers are concerned about how communications about the virus will be handled, admits Paul Sundberg, vice-president for science and technology for the National Pork Board, who says his group has already met with officials at the Centers for Disease Prevention and Control in Atlanta to discuss the naming challenging.
The above comments from the Helen Branswell piece in Scientific American, misrepresent the history of influenza evolution in swine. The trH1N1 which caused the 2009 pandemic was commonly called “swine flu” because it represented one of the many serotypes that circulated in swine (which had various numbers of classical swine genes), just as the H1N1 that circulated in humans prior to the pandemic was called seasonal H1N1, and the H3N2 in humans is called seasonal H3N2.
The flu viruses in swine (swine flu or SOIV’s – Swine Origin Influenza Viruses) in the United States began to get much more complex in the early 1990’s. The first influenza isolated was from a pig in Iowa in 1930 and was the H1N1 serotype. This lineage, which began to be challenged in the early 1990’s, is called “classical swine”. In the early 1990’s a pig was co-infected with classical H1N1 and seasonal H3N2, to produce a double reassortant, with PB1, HA, and NA from (human) seasonal H3N2. Thus, the virus had 3 human flu gene segments and 5 classical swine gene segments. This virus circulated in swine, so like classical H1N1, it was another swine flu serotype (just as humans had two co-circulating serotypes, H1N1 and H3N2,) but these were very different lineages. The human seasonal H1N1 traces back to the first human flu isolate from a scientist in England in 1933. Although seasonal H1N1 and classical swine H1N1 have the same serotype, they are distinct lineages which had been more closely related than they are currently, but did have enough similarity so the elderly had some protection against pandemic H1N1 because of prior infections with seasonal H1N1 from the 1920’s, 30’s 40’s, and 50’s.
In the late 1990’s the swine flu’s became more complex when a pig was infected with the H3N2 double reassortant and an avian influenza virus. Two more of the swine gene segments, the two polymerases that were classical swine, were exchanged for the avian polymerase, which created the H3N2 triple reassortant (trH3N2), which had three human flu genes (PB1, HA, NA), two avian genes (PB2 and PA), and three swine genes (NP, MP, NS). This trH3N2 is the precursor to the virus under discussion, although it went through one more change which exchanged the human N2 from the early 1990’s with the human N2 from 2003, so the constellation of genes remains the same, except the N2 is from human seasonal flu circulating in 2003, while the H3 is from the early 1990’s.
These relationships can be can be seen in the HA and NA phylogenetic trees in the CDC (Nancy Cox) presentation at the FDA vaccine advisory committee, which shows the H3 tracing back to seasonal H3 from the 1990’s in slide 6 and the N2 tracing back to seasonal H2 from 2003 in slide 7.
However, swine flu or SOIV’s (Swine Origin Influenza Viruses) are complex because triple reassortants involved multiple swaps with the external genes (HA and NA) to create various triple reassortant serotypes. All of these viruses maintain the polymerase complex formed in the 1990’s which has a human PB1 (from seasonal H3N2), and two avian polymerase gens (PB2 and PA), and various numbers of swine genes depending of the origin of the HA and NA genes.
The 2009 pandemic was a triple reassortant, which had swapped the human H3 and N2 for swine H1 and N1. Thus, it was a trH1N1, while other SOIVs which just swamped the human H3 for swine H1 were trH1N2. Thus, there is no problem distinguishing the triple reassortant H1N1 (trH1N1) from seasonal H1N1, or trH3N2 from seasonal H3N2. The pandemic trH1N1 was named H1N1pdm09 to distinguish it from other trH1N1’s and to reflect the fact that it caused the 2009 pandemic (pandemic is abbreviated pdm and 2009 is abbreviated 09). The current trH3N2 in 2011 evolved from the trH3N2 in humans in 2010, which also acquired the H1N1pdm09 M gene. Although WHO has not yet declared the pandemic, when it does, the official name will be H3N2pdm11. Until then it is trH3N2 with a H1N1pdm09 M gene, but there is no need to add S-O to the tr, which, as described above, has a very well known swine origin.
The CDC wants to use S-O to maintain its “swine exposure” narrative, which has no real basis for the 2011 trH3N2 with H1N1pdm09, which should be called H3N2pdm11 because it is transmitting in humans in a sustained manner, but the abysmal CDC surveillance targets those with swine exposure. Consequently, there has only been 12 influenza A positive samples sequences since July 2011 from those under 10, and 9 of the 12 have been H3N2pdm11 because the virus is transmitting in humans, but is most easily detected in those under 10 which account for 9 of the 10 confirmed cases in 2011.
If the CDC targeted those under 10 by aggressively testing influenza A positive cases, instead of those with “swine exposure”, the extent of spread among those without swine exposure would be much clearer than the data produced by the CDC biased testing, which targets those with swine exposure in the off season, and has yet to significantly increase surveillance in those under 10 via PCR testing and sequencing of most influenza A positive samples.
Recombinomics
Presentations
Recombinomics
Publications
Recombinomics
Paper
at Nature Precedings