Figure 1
Figure 1. Strategy for the ablation of p12, p30, and HBZ and characterization of the mutant viruses and cell lines. (A) Genetic organization of the HTLV-1 provirus genome and schematic representation of the overlapping orf I-IV (top). Amino acid changes in the mutant molecular clones (bottom). LTR indicates long terminal repeat. (B) Level of p19 Gag produced in the supernatants of the 729 B cell–infected cell lines measured by enzyme-linked immunoabsorbent assay. (C) Western blot analysis of the cell lysates from the 729 B-cell lines infected with the HTLV-1 mutant viruses with the use of antibodies to p24 Gag and to Tax. An antibody to tubulin was used as a control for equal loading of proteins. (D) Southern blot analysis of genomic DNA from the infected 729 B-cell lines. The numbers on the right represent the migration of the molecular weight (MW) marker.

Strategy for the ablation of p12, p30, and HBZ and characterization of the mutant viruses and cell lines. (A) Genetic organization of the HTLV-1 provirus genome and schematic representation of the overlapping orf I-IV (top). Amino acid changes in the mutant molecular clones (bottom). LTR indicates long terminal repeat. (B) Level of p19 Gag produced in the supernatants of the 729 B cell–infected cell lines measured by enzyme-linked immunoabsorbent assay. (C) Western blot analysis of the cell lysates from the 729 B-cell lines infected with the HTLV-1 mutant viruses with the use of antibodies to p24 Gag and to Tax. An antibody to tubulin was used as a control for equal loading of proteins. (D) Southern blot analysis of genomic DNA from the infected 729 B-cell lines. The numbers on the right represent the migration of the molecular weight (MW) marker.

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