Figure 6
Figure 6. The role of SR-BI and lectins in HCV association and B-cell transinfection. CD40L/IL-4–stimulated PBMC-derived primary B cells were incubated with (A) scavenger receptor inhibitors fucoidin and poly-I or the respective control molecules chondroitin or poly-C, mannan, or EDTA for 1 hour at 37°C and (B) anti-CD81, anti–SR-BI, anti–DC-SIGN/L-SIGN, and control antibodies (10 μg/mL) for 1 hour on ice. B cells were washed to remove inhibitors and unbound antibodies and incubated with JFH-1 for 2 hours at 37°C, the virus was removed by washing, the cells were cocultured with Huh-7.5, and transinfection was quantified. Data represent the SD FFUs per 106 B cells from 3 replicate infections. Percentage inhibition of transinfection compared with control molecules or isotype control antibodies are noted for each treatment.

The role of SR-BI and lectins in HCV association and B-cell transinfection. CD40L/IL-4–stimulated PBMC-derived primary B cells were incubated with (A) scavenger receptor inhibitors fucoidin and poly-I or the respective control molecules chondroitin or poly-C, mannan, or EDTA for 1 hour at 37°C and (B) anti-CD81, anti–SR-BI, anti–DC-SIGN/L-SIGN, and control antibodies (10 μg/mL) for 1 hour on ice. B cells were washed to remove inhibitors and unbound antibodies and incubated with JFH-1 for 2 hours at 37°C, the virus was removed by washing, the cells were cocultured with Huh-7.5, and transinfection was quantified. Data represent the SD FFUs per 106 B cells from 3 replicate infections. Percentage inhibition of transinfection compared with control molecules or isotype control antibodies are noted for each treatment.

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