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. 2013 Oct 22;4(5):e00803-13. doi: 10.1128/mBio.00803-13

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Copyright © 2013 Xu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

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FIG 5 — HPIV3-HN_Q552/R559/F_D396 has enhanced fitness for growth in HAE compared to HPIV3-HN_H552 (reference strain) and HPIV3-HN_Q552. HAE cultures were coinfected with 4,000 PFU of the HPIV3 reference strain and HPIV3-HN_Q552/R559/F_D396 (a) or of HPIV3-HN_Q552 and HPIV3-HN_Q552/R559/F_D396 (b) at the ratios indicated. Viral titers (left) were determined at 1, 2, and 3 days postinfection. The ratios of viral genomes released (right) containing the codon CAA (glutamine) or CGA (arginine) corresponding to residue 559 on HN were quantified by qRT-PCR by SNP genotyping. The HPIV3 reference strain and HPIV3-HN_Q552 genomes carried Q559, while HPIV3 small plaques (HPIV3-HN_Q552/R559/F_D396) carried R559. Titers on days 1 to 3 after HAE infection were determined by plaque assay in CV1 cells based on plaque size. Viral genome was quantified using SNP genotyping specific to Q or R at position 559 in HN. All data points are means and standard deviations (SD) from triplicate experiments.