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Additionally, viral proteins may also play a role in inducing a disruption of interendothelial junctions23 through mechanisms involving Src kinases, molecules required for vascular permeability during angiogenesis.24 In this way, Sanz-Cameno et al decribed for the first time the ability of hepatitis B virus (HVB), through HBx protein, to promote Ang-2 expression in liver tissue of chronically infected patients,25 and Lara-Pezzi et al found that matrix metalloproteinase 2 is also up-regulated by HBx protein.26 Binding between EC and ECM may be altered in the livers of chronic viral hepatitis patients.27 Integrin av• •3, expressed by activated EC, shows increased tissular expression in chronic hepatitis C (CHC).22 Interestingly, when EC are induced to migrate by HGF, integrin av• •3 accumumaltes at the leading edge,22 which represents the anchoring zone required for pulling the cellular body28(Table I)