North American Triple Reassortant and Eurasian H1N1 Swine Influenza Viruses Do Not Readily Reassort to Generate a 2009 Pandemic H1N1-Like Virus

Abstract

The 2009 pandemic H1N1 virus (pH1N1) was derived through reassortment of North American triple reassortant and Eurasian avian-like swine influenza viruses (SIVs). To date, when, how and where the pH1N1 arose is not understood. To investigate viral reassortment, we coinfected cell cultures and a group of pigs with or without preexisting immunity with a Eurasian H1N1 virus, A/Swine/Spain/53207/2004 (SP04), and a North American triple reassortant H1N1 virus, A/Swine/Kansas/77778/2007 (KS07). The infected pigs were cohoused with one or two groups of contact animals to investigate viral transmission. In coinfected MDCK or PK15 continuous cell lines with KS07 and SP04 viruses, more than 20 different reassortant viruses were found. In pigs without or with preexisting immunity (immunized with commercial inactivated swine influenza vaccines) and coinfected with both viruses, six or seven reassortant viruses, as well as the parental viruses, were identified in bronchoalveolar lavage fluid samples from the lungs. Interestingly, only one or two viruses transmitted to and were detected in contact animals. No reassortant containing a gene constellation similar to that of pH1N1 virus was found in either coinfected cells or pigs, indicating that the reassortment event that resulted in the generation of this virus is a rare event that likely involved specific viral strains and/or a favorable, not-yet-understood environment.

Expansion of Genotypic Diversity and Establishment of 2009 H1N1 Pandemic-Origin Internal Genes in Pigs in China

“…This is consistent with our earlier work (2,16,17), reports from other regions (38,39), and experimental coinfections of pigs with EA and TR viruses (40). At its emergence, the HA of pdm/09 virus was suggested to have been optimally adapted to humans, maintaining its receptor binding avidity via compensatory substitutions (41).…”

Pathogenicity and Transmissibility of Novel Reassortant H3N2 Influenza Viruses with 2009 Pandemic H1N1 Genes in Pigs

“…However, both the wild-type rgKS-107824 virus and the singly mutated rgKS-107824-G228S virus given at a low infection dose (10 4 TCID 50 /pig) were able to replicate in 3-week-old pigs until 7 days p.i. These data indicate that both virus and host factors, such as age and immune status, might influence viral replication, transmission, and evolution (49). It would be very interesting to compare the immune responses of the animals at different ages upon infection with influenza virus in future studies.…”

DAMPs and influenza virus infection in ageing

“…infection (Jain et al, 2009;Derek, 2009;Neumann et al, 2009;WHO, 2009;WHO, 2010;Vijaykrishna et al, 2010;Moreno et al, 2011;Dawood et al, 2012;Ma et al, 2014). Influenza is estimated to cause 36,000 deaths, > 200,000 hospitalizations and economic loss of 12-17 billion dollars during the annual outbreaks in the USA alone (Szucs, 1999;Thompson et al, 2003;Thompson et al, 2004;WHO, 2005).…”