In April 2009, the Centers for Disease Control and Prevention (CDC) at Atlanta reported that a new influenza virus was found in Mexico and the United States . The new influenza A H1N1 virus was soon characterized [2, 3] to be a triple reassortant derived from human, avian and swine influenza viruses [3–5]. The virus spread rapidly worldwide  and the World Health Organization (WHO) declared that the pandemic has reached phase 6 on June 11 2009 . Currently, the virus is still circulating worldwide .
Influenza viruses exhibit a restricted host range with limited replication in other species [8–10]. However, on rare occasions, influenza viruses can cross species barrier and adapt to a new host giving rise to a new lineage. Adaptation to a new species is believed to require multiple point mutations or reassortment of gene segments, or both. The molecular mechanism and genetic determinants that restrict, or permit, the replication of influenza viruses in humans remain unclear. While host haemagglutinin receptor specificity is clearly an important factor, it is not an absolute barrier to cross-species infection [11–13]. Growing evidence suggests that viral polymerase and nucleoprotein (NP) play a pivotal role in determining host selection and adaptation [13, 14].
Replication and transcription of influenza RNA segments are regulated by a virus-encoded RNA-dependent RNA polymerase . The polymerase is a heterotrimeric, multifunctional complex composed of three viral proteins, polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2), polymerase acidic protein (PA), which together with the viral NP form the viral ribonucleoprotein (vRNP) complex that is required for viral mRNA synthesis and replication . PA is an endonuclease [15–19], and involves in promoter and cap binding [20, 21]. PB1 contains active sites for nucleotide elongation [22, 23] and binding to promoters of vRNA and cRNA [22, 24, 25]. PB2 involves in cap-snatching from host mRNA [26, 27], and has been the focus of host adaptation and pathogenicity study. PB2 mutation, particularly the E627K, has been linked to the adaption of avian viruses to mammalian host [28, 29]. Another PB2 mutation, D701N, has been associated with increased virulence in mice [30, 31].
Given the current co-circulation of the 2009 pandemic H1N1 and seasonal H3N2 viruses, co-infection of these viruses in humans may occur . In this study, the polymerase activity of recombinant vRNP complexes that may be created from the reassortment between these two viruses was examined.