Fig. 5

Kudzu does not interfere with HIV-1 late replication events. a Kudzu has no activity on HeLa-CD4 cells chronically infected with NL4-3. Kudzu used at 1:400 dilution. Didehydro-Cortistatin A (dCA, a Tat inhibitor, 100 nM) was used as a control. Viral supernatants recovered 72 h post-infection from cells were assayed for their p24 antigen content. Data is the mean ± SD of 2 independent experiments. b Kudzu does not impact the transactivation activity of transfected Tat protein in TZM-bl cells. Tat mutated in the basic domain, Tat Mut, and buffer were used as negative controls. Luciferase activity per protein concentration was determined 48 h later. The data represents the mean ± SD of 2 independent experiments. c Schematic describing the mutation in Tat protein in U1 cells. d Kudzu has no activity on chronically-infected U1 cells before and after stimulation with SAHA (an histone deacetylase inhibitor, 1 μM). Kudzu used at 1:400 dilution. Flavopiridol (Flav., a CDK9 inhibitor, 100 nM) and Efavirenz (Efav., 100 nM) were used as controls. Viral supernatants recovered 72 h post-infection from cells were assayed for their p24 antigen content. Results are the mean ± SD of 3 independent experiments. e Kudzu has no activity on maturation and assembly of HIV-1 capsid. HIV-1 capsid originates from a 55 kDa Gag precursor proteolyzed into three folded proteins [matrix (MA), capsid (CA) and nucleocapsid (NC)] and 3 small peptides [spacer peptides 1 and 2 (SP1 and SP2) and p6]. HEK293T cells were transfected with NL4-3 in presence of compounds, and 72 h later, cell lysates were analyzed by western blot with anti-p24 antibody. Kudzu used at the dilution 1:400. Raltegravir (Ralt., 100 nM) and Saquinavir (300 nM) used as controls. The result are representative of 3 independent experiments