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. Author manuscript; available in PMC: 2017 Aug 10.
Published in final edited form as: Virology. 2016 Apr 20;494:89–99. doi: 10.1016/j.virol.2016.04.013

Figure 3. The polymerase complexes of H7N3 and H7N9 IAV affect pathogenesis.

Figure 3

Reassortant H7N3 and H7N9 viruses were generated by reverse genetics containing the three polymerase genes (PB2, PB1, and PA), the two glycoproteins (HA and NA), or the non-structural proteins (NS) from the reciprocal virus. (A) Female DBA/2J mice were infected with 103 TCID50 of H7N3 virus containing the PB2, PB1, PA (H7N35+3), or HA and NA (H7N36+2) or NS (H7N37+1) of the H7N9 virus, and morbidity and mortality were monitored for 21 days. (B) Female DBA/2J mice were infected with 103 TCID50 of H7N9 containing the PB2, PB1, PA (H7N95+3), or HA and NA (H7N96+2) or NS (H7N97+1) of the H7N3 virus, and morbidity and mortality were monitored for 21 days. (C) Female DBA/2J mice were infected with 102 TCID50 of H7N3 virus containing all three (H7N35+3) or individual polymerase gene-segments (H7N3 PB2N9, H7N3 PB1N9, H7N3 PAN9) of the H7N9 IAV and morbidity and mortality was monitored for 21 days. Each virus strain was tested in two or more separate experiments and includes at least seven animals per strain of IAV. * = P<0.05; ** = P<0.01; *** = P<0.001.