The inability to control the viral infection leads to the recruitment of inflammatory infiltrates into the liver parenchyma by IFN-γ-inducible CXCL-10 and -11 chemokines.27 Some of the results in the current study could be explained by the fact that INF-γ showed a declining trend while CXCL-10 and CXCL-11 levels increased in patients with moderate and severe inflammation compared to those without. This evidence concerns the gene CXCL11 and viral infectious disease.