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. 2009 Feb 20;5(2):e1000310. doi: 10.1371/journal.ppat.1000310

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Dreux et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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The SR-BI mutants tested were the SR-BI/CD36 chimera and the SES mutants, altering SR-BI intracellular domain, the Q402R/E418R, N173Q, and G420H-G424H mutants, altering SR-BI ectodomain. (A) Effect of SR-BI mutations on infectivity of HCVcc produced under standard conditions and assessed by measuring intracellular HCV RNA level at 72 hr post-infection (see Figure 2A). The results of infectivity (mean±SD; n = 3) are expressed relative to HCVcc infection of wt SR-BI–expressing SK-Hep1-CLDN1 cells, which was set to 100. (B) Results of HCVcc infection-enhancement induced by HDL (0.6 µg/ml cholesterol-HDL) on wt SR-BI–expressing SK-Hep1-CLDN1 cells, expressed as ratios relative to infection in the absence of HDL of the same cells set to 100 (mean±SD; n = 3). Similar experiments in BRL3A-CD81-CLDN1 cells expressing these SR-BI mutants were performed (data not shown) and were consistent with the results obtained in SK-Hep1-CLDN1 cells.