Volume 24, Number 1—January 2018
Dispatch
Mammalian Pathogenesis and Transmission of Avian Influenza A(H7N9) Viruses, Tennessee, USA, 2017
Figure 2

Figure 2. Replication kinetics of avian influenza A(H7N9) viruses in human respiratory tract cells, Tennessee, USA, 2017, compared with strains from Nebraska (gs/NE) and Asia (Anhui/1). Calu-3 cells (American Type Culture Collection, Manassas, VA, USA) were grown to confluence in 12-mm–diameter transwell inserts (Corning, Corning, NY, USA), infected apically with viruses shown at a multiplicity of infection of 0.01 (A and C) or 0.001 (B) 1 h, washed, and incubated at 37°C (A and B) or 33°C (C). Supernatants were removed at indicated times postinoculation, and titers of infectious virus were determined by titration in eggs. The limit of virus detection was 101.5 EID50/mL. Values are mean from triplicate independent cultures per virus. Error bars indicate SDs. *p<0.05 for HPAI vs. LPAI ck/TN viruses by 2-way analysis of variance with a Tukey posttest. EID50, 50% egg infectious dose; gs, goose; HPAI, highly pathogenic avian influenza virus; LPAI, low pathogenicity avian influenza virus.