Abstract
North American triple reassortant swine (TRS) influenza A viruses have caused sporadic human infections since 2005, but human-to-human transmission has not been documented. These viruses have six gene segments (PB2, PB1, PA, HA, NP, and NS) closely related to those of the 2009 H1N1 pandemic viruses. Therefore, understanding of these viruses' pathogenicity and transmissibility may help to identify determinants of virulence of the 2009 H1N1 pandemic viruses and to elucidate potential human health threats posed by the TRS viruses. Here we evaluated in a ferret model the pathogenicity and transmissibility of three groups of North American TRS viruses containing swine-like and/or human-like HA and NA gene segments. The study was designed only to detect informative and significant patterns in the transmissibility and pathogenicity of these three groups of viruses. We observed that irrespective of their HA and NA lineages, the TRS viruses were moderately pathogenic in ferrets and grew efficiently in both the upper and lower respiratory tracts. All North American TRS viruses studied were transmitted between ferrets via direct contact. However, their transmissibility by respiratory droplets was related to their HA and NA lineages: TRS viruses with human-like HA and NA were transmitted most efficiently, those with swine-like HA and NA were transmitted minimally or not transmitted, and those with swine-like HA and human-like NA (N2) showed intermediate transmissibility. We conclude that the lineages of HA and NA may play a crucial role in the respiratory droplet transmissibility of these viruses. These findings have important implications for pandemic planning and warrant confirmation.
Highlights
For nearly 70 years, swine influenza virus in North America was relatively stable, dominated by the classical-swine H1N1 subtype [1]
We wished to elucidate potential human health threats posed by the triple reassortant swine (TRS) viruses and to identify determinants of virulence in the TRS and closely related 2009 H1N1 pandemic viruses
We observed that the North American TRS viruses grew efficiently in both the upper and lower respiratory tracts and caused moderate pathogenicity in ferrets
Summary
For nearly 70 years, swine influenza virus in North America was relatively stable, dominated by the classical-swine H1N1 (cH1N1) subtype [1]. All of the currently circulating North American triple-reassortant swine (TRS) influenza A viruses contain a similar constellation of internal genes (avian PA and PB2, human PB1, and classical swine-lineage M, NP, and NS), but their surface glycoproteins are derived from different lineages (classical swine-lineage H1 and N1 and seasonal human-lineage H1, H3, N1 and N2). In 2009, TRS viruses with humanlike H1 and N1 (closely related to A/Brisbane/59/2007 [H1N1]) caused cough, fever, nasal congestion, rhinorrhea, sneezing, malaise, and dizziness in humans [9] These symptoms were very similar to those caused by the 2009 H1N1 pandemic viruses, which possessed six gene segments (PB2, PB1, PA, HA, NP, and NS) closely related to those of North American TRS viruses [10]. Unlike the 2009 H1N1 pandemic viruses, the TRS viruses were not reported to be transmissible among humans
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