Fig. 3.
Fig. 3. Conservation of ΔPstI mutation in ACH.p12I-transfectants at time of inoculation shown by PCR amplification of genomic DNA from ACH-, ACH.p12I-, and pKS- (vector control) transfected PBMC, MT-2 (HTLV-1-positive), and Jurkat (HTLV-1-negative) cells. The native (−) or Pst I-digested (+) 938 bp HTLV-1 ORF I/II-specific product is present in HTLV-1-positive cells and lacks the Pst I site corresponding to the ORF I exon 3 splice acceptor site in ACH.p12I-transfectants.

Conservation of ΔPstI mutation in ACH.p12I-transfectants at time of inoculation shown by PCR amplification of genomic DNA from ACH-, ACH.p12I-, and pKS- (vector control) transfected PBMC, MT-2 (HTLV-1-positive), and Jurkat (HTLV-1-negative) cells. The native (−) or Pst I-digested (+) 938 bp HTLV-1 ORF I/II-specific product is present in HTLV-1-positive cells and lacks the Pst I site corresponding to the ORF I exon 3 splice acceptor site in ACH.p12I-transfectants.

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