Skip to main content
. Author manuscript; available in PMC: 2015 Sep 17.
Published in final edited form as: FEBS Lett. 2014 Aug 14;588(18):3501–3510. doi: 10.1016/j.febslet.2014.08.009

Fig. 5.

Fig. 5

HCV core and conditioned media (CM) of HCV core-stimulated THP-1 macrophages and MDMs differentially affect reactivation of HIV-1 latent infection in U1 cells. (A) HCV core does not induce p24 production in U1 cells. U1 cells were stimulated with HCV core, β-galactosidase (negative control), or PMA (positive control) for 12 hours. Supernatants of stimulated U1 cells were assayed for p24 secretion by ELISA 24 hours after stimulation. (B) U1 cells show differential TNF-α production in response to TLR2/6 and TLR2/1 agonists. U1 cells were stimulated with PMA (positive control), HCV core, β-galactosidase protein, TLR2/6 agonist FSL-1, TLR2/1 agonist PAM3CSK4, and TLR2/2 agonist HKLM for 12 hours. Supernatants of stimulated U1 cells were assayed for p24 production by ELISA 24 hours after stimulation. (C) Stimulation of U1 cells with CM of HCV core-stimulated THP-1 macrophages and MDMs induced significant p24 production through the induction of the proinflammatory cytokines TNF-α and IL-6. U1 cells were stimulated with supernatants of HCV core–stimulated THP-1 macrophages and MDMs collected 14 hours after stimulation (CMs). Supernatants from U1 cells stimulated with CMs were assayed for p24 production by ELISA 24 hours after stimulation. Results from 3 independent experiments (THP-1 and U1) and CMs of 2 independent MDM donors are shown. Data are mean ± SD; *significantly different (P < 0.05) from control.