Figure 1

A model for HCV infection. A. HCV is present as a virus-lipoprotein complex in the human blood. HCV can be surrounded by several low density lipoproteins, so that the viral envelope proteins E1 and E2 might be masked. B. HCV is present within exosomes. It was recently shown that these exosomes are containing, apart from the genomic ribonucleic acid of HCV, the tetraspanin CD81 associated with E1 and E2. It is likely that the binding of the HCV-lipoprotein and/or the exosome-HCV complexes to the low density lipoprotein receptor (LDLr) might therefore be hampered in vitro by the cell-bound lipoproteins, or by the vast excess of free lipoproteins in the human blood. Therefore, it may be beneficial to remove the cell-bound lipoproteins with dextran sulfate (thus generating free LDL receptors) prior to the addition of the viral inoculum onto the target hepatocytes for the generation of an in vitro infection. The same may be true for the scavenger receptor SR-BI, since it does also bind LDL. In vivo, the use of statins may enhance the rate of HCV infection in HCV-infected patients, because of the increase of the LDL receptors at the surface of the hepatocytes.