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Commentary
Parallel
H1N1 Pandemics in 2010?
Recombinomics
Commentary 03:50
July 7, 2010
The above comments describe a swine H1N1 isolate from pigs at a 2007 Huron county fair in Ohio. In 2009 the sequences from the two confirmed cases, an exhibitor (10F) and her father (36M) were released. The two human HA sequences, A/Ohio/01/2007 and A/Ohio/02/2007, were identical to each other and from a triple reassortant with a human PB1, avian PB2 and PA and 5 North American swine sequences for the other five gene segments.
Recently a 2010 swine sequence from Iowa was released, A/swine/Iowa/03032/2010. It was most closely related to the two 2007 human sequences, but had acquired a number of non-synonymous polymorphisms found in 2009/2010 pH1N1 isolates including a duplication of G158E, a change associated with low reactors.
These developments have raised concerns of a second H1N1 pandemic.
The 2007 isolates almost caused a pandemic in 2007, based on the large number of fair attendees who developed respiratory symptoms in August, and the confirmation of swine H1N1 in the two cases described above. However, the lack of efficient transmission prevented the identification of additional cases.
The 2007 sequences had wild type sequences at positions 156-159 which represented an antigenic site that has led to immunological escape in 2009 pH1N1 isolates, while the 2010 isolate from Iowa has G158E, as well as a duplication of this polymorphism to produce a sequences of KKEKEN at the antigenic site, which will likely significantly blunt the effect of pre-existing antibodies directed against this site.
Prior 2010 swine sequences demonstrated pH1N1 transmission from swine to swine in the United States and G158E frequencies are increasing. This transmission in swine has led to the acquisition of a number of polymorphisms by the Iowa sequence, raising concerns that the new acquisitions, coupled with changes and duplication at position 158, will create a new H1N1 that is efficiently transmitted in humans, which would create distinct, but co-circulating pH1N1 species in humans.
The acquisition of the pH1N1 polymorphisms by swine H1N1 has remarkable parallels with the 1918 pandemic. The 1918 sequence have alternating regions of Iowa swine and human H1N1 polymorphisms generated by recombination. The similar evolution in 2010 Iowa swine sequences is cause for concern. Moreover, since pH1N1 and Iowa swine H1N1 share polymorphisms, distinctions may require sequencing, which is currently at a low level. An increase in swine and human surveillance, including sequencing, are dictated by the striking acquisitions by the swine sequence from Iowa.
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