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. 2013 Oct 19;21(4):S52–S58. doi: 10.1016/j.jfda.2013.09.034

Fig. 2.

Fig. 2

Sanguisorba officinalis extract (SOE) inhibits HIV-1 infection by binding to the viral envelope and blocking entry of the virus. (A) Post entry assay. GHOST-CD4-CCR5 or CXCR4 cells were coincubated with pseudovirus for 2 hours, washed, and then treated with the presence of 50 μg/mL SOE, dimethyl sulfoxide (DMSO) as negative control and 1 μM AZT as positive control for 48 hours. SOE does not inhibit either HIV-1ADA or HIVHxB2 virus gene replication after viral entry is achieved. (B) SOE-virus interaction assay. HIV-1ADA and HIVHxB2 pseudovirus pre-treated with 50 μg/mL SOE or DMSO as a negative control and entry inhibitor enfuvirtide (T-20) as a positive control. SOE pretreatment inhibited both HIVADA and HIVHxB2 pseudovirus infection to a similar degree as T-20. (C) SOE-cell binding assay. GHOST cells were pretreated with SOE or the CCR5 antagonist maraviroc and the CXCR4 antagonist JM2987 as positive controls, and DMSO as negative control for 1 hour at 37°C prior to being infected with HIV-1ADA or HIV-1HxB2. SOE pretreatment with the cells had no antiviral effect, whereas maraviroc and JM2987 pretreatment showed strong inhibition against HIV-1 ADA and HXB2 pseudoviruses at 1 μM, as expected. The data represent the mean ± standard deviation of triplicate experiments.