Abstract
Influenza viruses that express reporter proteins are useful tools, but are often attenuated. Recently, we found that an influenza virus encoding the Venus fluorescent protein acquired two mutations in its PB2 and HA proteins upon mouse adaptation. Here, we demonstrate that the enhanced viral replication and virulence in mice of this Venus-expressing influenza virus are primarily conferred by the PB2-E712D mutation, with only a minor contribution by the HA-T380A mutation.
Highlights
Recombinant influenza A viruses that express reporter proteins are useful tools for studying the dynamics of influenza virus infection in vivo[1,2]
These data indicate that the PB2-E712D and HA-T380A mutations both contributed to increased virus replication in Madin-Darby canine kidney (MDCK) cells
In mice infected with 103–105 plaque-forming units (PFU) of viruses, MA-Venus-PR8 was more virulent than WT-Venus-PR8, as reported previously[4] (Fig. 1B)
Summary
Recombinant influenza A viruses that express reporter proteins are useful tools for studying the dynamics of influenza virus infection in vivo[1,2]. We infected Madin-Darby canine kidney (MDCK) cells at a multiplicity of infection (MOI) of 0.001 and determined viral titers in supernatants by using plaque assays (Fig. 1A). These data indicate that the PB2-E712D and HA-T380A mutations both contributed to increased virus replication in MDCK cells.
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