Antisense oligonucleotide-mediated activation or suppression of HIV-2, SIV and HIV-1 RNA tight dimerization. A. Schematic representation of the leader RNAs as described in Figure 1 with the oligonucleotide binding sites indicated (left panel, HIV-2 or SIV, right panel, HIV-1). B. 1–561 HIV-2 (left), 1–550 SIV (center) and 1–373 HIV-1 (right) RNAs were incubated at 55°C for 30 minutes in their respective dimer buffers with or without a 20-fold molar excess of antisense oligonucleotides directed against the C-box or G-box elements (Table 2) before loading on a TBE/26°C agarose gel. The 5' end of all asG oligonucleotides bind to the start codon of the gag gene in the G-box element and thus to the majority of nucleotides involved in the CGI structures (8 nts out of 13, Figure 1F). The asC oligonucleotides bind to all (HIV-2 and SIV) or most (HIV-1, 10 nts out of 13) of lentiviral C-box elements (Figure 1F). Lanes 1, 5, 6, 10, 11 and 15 correspond to RNA incubated in dimer buffer at 55°C without oligonucleotide. The monomer and dimer RNA species are indicated by M and D, respectively. C. 1–561 HIV-2 (left), 1–550 SIV (center) and 1–373 HIV-1 (right) RNAs were incubated at 55°C for 30 minutes in dimer buffer with or without a 20-fold excess of antisense oligonucleotides directed against sequences upstream of SL1 and including stem B (asΨ in HIV-2 and SIV, as246 in HIV-1) or the loop and 5' stem of SL1 (asSL1) before loading on a TBE/26°C agarose gel.