Fig. 5

The formation of G-based hyperstructures contributes to ODN A’s antiviral activity. a ODN A, ODN Co and ODN G (8 μM) were incubated for 1 h in PBS and analyzed by native polyacrylamide gel electrophoresis. b ODN A, ODN Co, ODN G (250 nM) or buffer alone were incubated together with HIV-1 particles (1 × 10⁹) for 6 h at 37 °C. Following infection of Jurkat 1G5 T cells, release of p24 antigen was detected over time in the culture supernatants (day 3–21 post infection). Two-way ANOVA followed by Bonferroni posttest was used for statistical evaluation. ODN A-mediated inhibition (as compared to buffer alone) was highly significant (p < 0.001) at day 10–21 post infection. ODN G-mediated inhibition (as compared to buffer alone) was highly significant (p < 0.001) at day 10, 14 and 21 post infection. c Following the experimental design depicted at the left, HEK293T cells were transfected with plasmid vectors expressing HIV-1 Env and Tat, or the parental vector (pcDNA) as a negative control. At 24 h post transfection, Jurkat 1G5 reporter T cells, which were pre-incubated for 1 h in 500 nM ODN or buffer alone (negative control) were added to the HEK293T cell cultures for another 24 h. Jurkat 1G5 T cell-derived luciferase signals were subsequently measured, indicating successful cell fusion. One-way ANOVA followed by Dunnett’s Multiple Comparison Test was used for statistical evaluation. ODN A-and ODN G-mediated cell fusion (as compared to buffer alone) was highly significant (p < 0.001). d Different concentrations of ODN A or ODN G were pre-incubated with HIV-1 as before. Subsequently, Jurkat 1G5 T cells were infected and HIV-1 p24 antigen release was detected at day 7 post infection. EC₅₀ values were calculated using GraphPad PRISM (Graphpad Software, Inc, USA) software