The I30T mutation in NS2 enhances the efficiency of <i>trans</i> complementation in a genotype-specific manner.

<p>(A) Organization of the chimeric H/J-NS2 replicon expression product, showing the location of the compensatory I30T mutation in the H77-derived sequence <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000403#ppat.1000403-Yi2" target="_blank">[14]</a>,<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000403#ppat.1000403-Kalinina2" target="_blank">[36]</a>. See also <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000403#ppat-1000403-g002" target="_blank">Figure 2A</a>. (B) Immunoblot detection of NS2 protein using anti-Myc antibodies. (C,D) Infectious virus yields after transfection of (C) JFH1(SA) or (D) HJ3-5(SA) RNA into VEE replicon cells expressing GFP, or Myc-H/J-NS2 with or without the I30T mutation. Extracellular virus yields were determined three days following transfection. The detection limit of the infectivity assay is indicated by the broken line.