Although exogenous PER2 overexpression reduced the apparently coherent elevated levels of Mx1 and IRF9 in OR6 replicating the HCV RNA, we assume that some viral components act to modulate viral load by means of the activation or inhibition of host defense proteins in order to maintain low steady levels of virus in the infected cells, enabling HCV to escape from the host immune surveillance, and facilitating persistent viral infection. The gene discussed is MX1; the disease is viral infectious disease.