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. 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. 2.

Fig. 2

HCV core enhances HIV-1 infectivity via TLR2. THP-1 macrophages (A) and MDMs (B) were infected with a luc-reporter, macrophage-tropic BaL HIV-1 pseudotype. Cells were unstimulated or stimulated with 5 μg/ml of HCV core or β-Gal recombinant protein control in the presence of a neutralizing human monoclonal anti-TLR2 Ab or isotype control (Invivogen) 12 hours after infection. Luc activity was measured 2 days after infection and results from 3 independent experiments (THP-1) and 2 independent MDMs donors are shown. Luciferase activity in cell lysates was measured as relative light units per second. Results represent means ± SD. To determine the role of MAP kinases in HCV core-mediated enhancement of HIV infection in THP-1 macrophages (C) and MDMs (D), cells were prestimulated with specific inhibitors of JNK (50 μM SP600125), p38 (20 μM SB203580), and MEK1/2 (50 μM PD98059, and 20 μM U0126) for 30 minutes and then infected with HIV-1 BaL pseudotype. Infected cells were left unstimulated or treated with HCV core or β-Gal 12 hours after infection. Luc activity was measured 2 days after infection and results from 3 independent experiments (THP-1) and 2 independent MDM donors are shown. Luciferase activity in cell lysates was measured as relative light units per second. Data are shown as relative luciferase units (RLU) of HIV infectivity (mean ± SD). Values that were significantly different (P < 0.05) from the value of HIV-infection alone group are indicated (*).