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. 1999 Sep;73(9):7421–7429. doi: 10.1128/jvi.73.9.7421-7429.1999

FIG. 2.

FIG. 2

FIG. 2

Site-directed mutations in the upstream copy of dr1. The six substitution mutations shown in boldface in panel A and circled in panel B (M3, M3A, M3B, M4, M5, and ML2) resulted in at least a 10-fold reduction in viral replication compared to the wild type (Fig. 3). The remaining seven dr1 mutants failed to cause a permanent reduction in viral replication. (A) Aligned sequences of the upstream copy of dr1 from Pr-RSV-C nt 6897 to 6989 and the mutations studied here. Dashes indicate sequence identity. (B) Predicted secondary structure of dr1. The structure was predicted by using M-fold (34). The approximate locations of the mutations are indicated.