Abstract
Pandemic H1N1/2009 influenza virus, derived from a reassortment of avian, human, and swine influenza viruses, possesses a unique gene segment combination that had not been detected previously in animal and human populations. Whether such a gene combination could result in the pathogenicity and transmission as H1N1/2009 virus remains unclear. In the present study, we used reverse genetics to construct a reassortant virus (rH1N1) with the same gene combination as H1N1/2009 virus (NA and M genes from a Eurasian avian-like H1N1 swine virus and another six genes from a North American triple-reassortant H1N2 swine virus). Characterization of rH1N1 in mice showed that this virus had higher replicability and pathogenicity than those of the seasonal human H1N1 and Eurasian avian-like swine H1N1 viruses, but was similar to the H1N1/2009 and triple-reassortant H1N2 viruses. Experiments performed on guinea pigs showed that rH1N1 was not transmissible, whereas pandemic H1N1/2009 displayed efficient transmissibility. To further determine which gene segment played a key role in transmissibility, we constructed a series of reassortants derived from rH1N1 and H1N1/2009 viruses. Direct contact transmission studies demonstrated that the HA and NS genes contributed to the transmission of H1N1/2009 virus. Second, the HA gene of H1N1/2009 virus, when combined with the H1N1/2009 NA gene, conferred efficient contact transmission among guinea pigs. The present results reveal that not only gene segment reassortment but also amino acid mutation were needed for the generation of the pandemic influenza virus.
Highlights
Pandemic H1N1/2009 influenza virus spread by human-tohuman transmission across the globe at an unprecedented rate after it was first detected in humans [1,2]
Generation and in vitro characteristics of rH1N1 virus Our previous study found that the NA and M genes of a Eurasian avian-like H1N1 swine influenza virus, A/swine/Fujian/ 204/2007 (Eurasian-204, accession numbers: FJ536810-FJ536817) [16] and the other six genes of a triple-reassortant H1N2 swine influenza virus A/swine/Guangdong/1222/2006 (Triple-1222, accession numbers: GU086078-GU086085) [8] belonged to the same cluster of H1N1/2009 viruses in the phylogenetic tree
PBJ09 virus showed efficient transmission that all four exposed animals were detected to be positive, while H1N1 influenza virus A/Tianjin/15/2009 (hTJ15) transmitted less efficiently than pBJ09 with two of four exposed animal becoming infected. These results indicated that rH1N1 virus has a pathogenicity that is similar to H1N1/2009 virus in mice, it does not acquire the transmissibility in guinea pigs which is a typical trait of H1N1/2009 virus
Summary
Pandemic H1N1/2009 influenza virus spread by human-tohuman transmission across the globe at an unprecedented rate after it was first detected in humans [1,2]. Genetic analyses revealed that the pandemic H1N1/2009 influenza viruses possessed a unique combination of gene segments from swine, human and avian origins; containing PB2 and PA genes of North American avian virus origin, the PB1 gene of human H3N2 virus origin, HA, NP and NS genes of classical swine H1N1 virus origin, and NA and M genes of Eurasian avianlike swine virus origin [6,7]. These genes have been already established in the triple-reassortant H1N2 and H1N1 swine viruses in North America and in the Eurasian avian-like swine H1N1 viruses for more than 10 years [8,9,10,11]. H1N1/2009 was probably a result of an immediate reassortment between two or more swine viruses, i.e. triple-reassortant H1N2 (or H1N1) and the Eurasian avian-like H1N1 swine viruses [7,12,13,14]
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