Since HCV particles can potentially bind both LDL receptor and SRB1, one can wonder what would
preferentially orient HCV entry towards a productive infection by interacting with SRB1 instead of the
LDL receptor. One possibility is that the particular lipid and apolipoprotein composition of the virion
circulating in the bloodstream endows the virus with a higher affinity for SRB1. Furthermore, since HCV
glycoprotein E2 also interacts with SRB1, it is possible that HCV binding to SRB1 is stabilized by this
interaction before transferring the virion to the next receptor. However, one cannot exclude that virion
remodeling by lipoprotein lipase in the bloodstream could also lead to some binding to the LDL receptor.