Submitted to: American Society for Virology Meeting
Publication Type: Abstract only
Publication Acceptance Date: 4/11/2006
Publication Date: 7/15/2006
Citation: Ma, W., Lekcharoensuk, P., Lager, K.M., Webby, R., Yoon, K., Richt, J.A. 2006. The role of avian influenza polymerase genes in the adaptation of swine influenza virus to pigs [abstract]. American Society for Virology. Paper No. P30-5. p. 278-279. Interpretive Summary:
Technical Abstract: Swine influenza is caused by influenza A viruses that have a remarkable ability for genetic change due to genetic drift and shift. To date, 16 HA and 9 NA subtypes of influenza A viruses are known to exist and several of these subtypes are capable of infecting pigs. Essentially, all swine influenza virus (SIV) isolates in the Unite States prior to 1998 were of one subtype, the “classical” H1N1 (cH1N1) subtype. Around 1998 reassortment events occurred in pigs which resulted in the transfer of avian and human influenza genes into cH1N1 SIVs, producing novel H3N2, H1N2 as well as reassortant H1N1 (rH1N1) viruses. These novel H3N2, H1N2 and rH1N1 viruses are now widespread in the U.S. swine population and rH1N1 viruses appear more virulent than cH1N1 SIVs. Typically, the polymerase complex of these novel viruses consists of 2 avian polymerase genes (PA, PB2) and 1 human polymerase gene (PB1). We hypothesize the novel viral polymerase genes are the basis for better adaptation and increased virulence of reassortant SIVs for pigs. To test this hypothesis, a reverse genetic system for a cH1N1 SIV (A/Swine/IA/15/30,) was established (rg1930). The rg1930 system was used to rescue reassortant SIVs that have avian and/or human polymerase gene(s) instead of swine polymerase genes. The growth characteristics of the rescued viruses in MDCK and PK-15 cells were compared to that of the parental virus. Seven reassortant SIVs containing avian and/or human polymerase genes (rPA, rPB1, rPB2, rPA/PB1, rPA/PB2, rPB1/PB2, rPA/PB1/PB2) were rescued with the rg1930 background. The rPA and rPA/PB2 formed larger plaques than did rg1930 and the other reassortant SIVs. While the rg1930 and all reassortant SIVs grew to similar titers in MDCK (canine kidney) cells, the rPA and rPA/PB2 grew to higher titers in PK-15 (porcine kidney) cells in comparison to the parental and the other reassortant viruses. These results suggest acquiring avian polymerase gene(s) plays an important role for replication in porcine cells and most likely for the pathogenesis of SIV in pigs.