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. 2004 Oct;78(20):11288–11295. doi: 10.1128/JVI.78.20.11288-11295.2004

FIG. 7.

FIG. 7.

Genetic disruption of NS4B's NBM impairs HCV RNA replication. Replication of HCV replicons harboring the mutations depicted in Fig. 5B were assayed by colony formation assays. (A) Wild-type and mutant replicons were electroporated into Huh-7 cells, and G418-resistant colonies were selected and stained with crystal violet. These replicons contain the gene for neomycin phosphotransferase (6). Each dot represents a colony of Huh-7 cells that was able to grow in the presence of G418 due to the presence of efficiently replicating intracellular replicons. WT, Bart79I (wild type) (3, 6); Pol−, Bart79I with a lethal mutation in NS5B (16); KR, Bart79I with a Lys135Arg point mutation; KS, Bart79I with a Lys135Ser point mutation; GV, Bart79I with a Gly129Val point mutation; IN, Bart79I with an Ile131Asn point mutation. A representative plate is shown. (B) Percentages of colonies relative to wild-type control. Note that rare colonies were obtained with the G129V mutant protein (*) and that none were obtained with the Pol− or I131N mutant proteins.