Multiple reassortment between pandemic (H1N1) 2009 and endemic influenza viruses in pigs, United States.

As a result of human-to-pig transmission, pandemic influenza A (H1N1) 2009 virus was detected in pigs soon after it emerged in humans. In the United States, this transmission was quickly followed by multiple reassortment between the pandemic virus and endemic swine viruses. Nine reassortant viruses representing 7 genotypes were detected in commercial pig farms in the United States. Field observations suggested that the newly described reassortant viruses did not differ substantially from pandemic (H1N1) 2009 or endemic strains in their ability to cause disease. Comparable growth properties of reassortant and endemic viruses in vitro supported these observations; similarly, a representative reassortant virus replicated in ferrets to the same extent as did pandemic (H1N1) 2009 and endemic swine virus. These novel reassortant viruses highlight the increasing complexity of influenza viruses within pig populations and the frequency at which viral diversification occurs in this ecologically important viral reservoir.

Genetic composition of contemporary swine influenza viruses in the West Central region of the United States of America.

BACKGROUND: Because of continuous circulation in different animal species and humans, influenza viruses have host-specific phenotypic and genetic features. Reassortment of the genome segments can significantly change virus phenotype, potentially generating virus with pandemic potential. In 2009, a new pandemic influenza virus emerged. OBJECTIVES: In this study, we attempted to find precursor viruses or genes of pandemic H1N1 influenza 2009 among 25 swine influenza viruses, isolated in the West Central region of the United States of America (USA), between 2007 and 2009. The Phylogenetically Similar Triple-Reassortant Internal Genes (PSTRIG) cassette of all the viruses studied here as well as the PSTRIG cassette of pandemic H1N1 viruses have close but equidistant phylogenetic relationships to the early triple-reassortant swine H3N2 influenza A isolated in the USA in 1998. METHODS: Samples (nasal swabs and lung tissue lavage) were taken from swine with or without clinical signs of respiratory disease via farmer-funded syndromic surveillance. All studied viruses were isolated in Madin-Darby Canine Kidney cell cultures from the above-mentioned samples according to standard protocols recommended for influenza virus isolation. Sequences were obtained using BigDye Terminator v3.1 Cycle Sequencing kit. Phylogenetic trees were built with MEGA 4.0 software using maximum composite likelihood algorithm and neighbor-joining method for tree topology reconstruction. RESULTS: Among the 25 viruses studied, we have not found any gene segments of Eurasian origin. Our results suggest that pandemic H1N1 viruses diverged and are not directly descended from swine viruses that have been circulating in USA since 1998.

Diversity of influenza viruses in swine and the emergence of a novel human pandemic influenza A (H1N1).

The novel H1N1 influenza virus that emerged in humans in Mexico in early 2009 and transmitted efficiently in the human population with global spread has been declared a pandemic strain. Here we review influenza infections in swine since 1918 and the introduction of different avian and human influenza virus genes into swine influenza viruses of North America and Eurasia. These introductions often result in viruses of increased fitness for pigs that occasionally transmit to humans. The novel virus affecting humans is derived from a North American swine influenza virus that has acquired two gene segments [Neuraminidase (NA) and Matrix (M)] from the European swine lineages. This reassortant appears to have increased fitness in humans. The potential for increased virulence in humans and of further reassortment between the novel H1N1 influenza virus and oseltamivir resistant seasonal H1N1 or with highly pathogenic H5N1 influenza stresses the need for urgent pandemic planning.