In in vitro studies, CD81 has been shown to be an entry receptor for HCV and could be involved in infection of B cells by the virus.26In vitro, infection of B-cell lines with HCV leads to somatic mutations of several oncogenes and tumor suppressor genes such as p53, beta-catenin and Bcl6.27,28 The expression of the HCV core protein (C) and non-structural protein 3 (NS3) has been associated with the induction of nitric oxide synthase (NOS) which might be responsible for these mutations (Figure 3A). This evidence concerns the gene CD81 and infection.