Abstract
Since emergence of the pandemic (H1N1) 2009 virus in April 2009, three influenza A viruses—seasonal (H3N2), seasonal (H1N1), and pandemic (H1N1) 2009—have circulated in humans. Genetic reassortment between these viruses could result in enhanced pathogenicity. We compared 4 reassortant viruses with favorable in vitro replication properties with the wild-type pandemic (H1N1) 2009 virus with respect to replication kinetics in vitro and pathogenicity and transmission in ferrets. Pandemic (H1N1) 2009 viruses containing basic polymerase 2 alone or in combination with acidic polymerase of seasonal (H1N1) virus were attenuated in ferrets. In contrast, pandemic (H1N1) 2009 with neuraminidase of seasonal (H3N2) virus resulted in increased virus replication and more severe pulmonary lesions. The data show that pandemic (H1N1) 2009 virus has the potential to reassort with seasonal influenza viruses, which may result in increased pathogenicity while it maintains the capacity of transmission through aerosols or respiratory droplets.
Highlights
The influenza virus A (H1N1) that caused the first influenza pandemic of the 21st century, pandemic (H1N1) 2009, continues to be detected worldwide [1,2]
Subtype H1N2 reassortant influenza viruses that contain the HA of seasonal influenza A (H1N1) and the NA of seasonal influenza A (H3N2) viruses have been isolated from humans during previous influenza seasons, confirming that such HA/NA combinations can emerge in humans [15,16]
Upon repeating the procedure 4 times for both reassortment combinations, the seasonal influenza virus genes that were selected in the pandemic (H1N1) 2009 virus backbone were more or less consistent, with NA of seasonal influenza virus A (H3N2) being selected in 4/4 attempts, PB1 of seasonal influenza A (H3N2) and PB2 of seasonal influenza virus A (H1N1) in 3/4 attempts, and PA of seasonal influenza virus A (H1N1) in 2/4 attempts
Summary
The influenza virus A (H1N1) that caused the first influenza pandemic of the 21st century, pandemic (H1N1) 2009, continues to be detected worldwide [1,2]. Cocirculation of multiple strains of influenza virus A in humans provides an opportunity for viral genetic reassortment (mixing of genes from >2 viruses) [10]. Genetic reassortment of pandemic (H1N1) 2009 virus with seasonal influenza A (H3N2) or seasonal influenza A (H1N1) viruses might represent a route to enhanced pathogenicity. No reassortment events between pandemic (H1N1) 2009 and seasonal viruses have been reported in humans. A triple-reassortant swine influenza virus A (H1N1), distinct from pandemic (H1N1) 2009 virus and containing the hemagglutinin (HA) and NA genes of seasonal influenza virus A (H1N1), was described recently [11]. To investigate the potential for reassortment between seasonal influenza A and pandemic (H1N1) 2009 viruses, we used an in vitro selection method using reverse genetics and serial passaging under limited dilution conditions. We report here the identification of 4 reassortants with different gene constellations
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