To further support this hypothesis, direct infection of lymphocytes by HCV would not be necessary in vivo to induce somatic mutations of several oncogenes and tumor suppressor genes such as p53, beta-catenin and Bcl6 as recombinant HCV E2 binding to surface CD81 has also been shown to induce somatic hypermutation of the immunoglobulin gene locus (Figure 3B).41 As the E2 glycoprotein is expressed on the virion surface, this mechanism of mutagenesis would not require direct infection of B cells by HCV. Here, TP53 is linked to infection.