The replication of HCV in various lymphoid and hepatocellular cell lines suggests that these cell types are permissive for HCV replication. Lymphotrophism has been further documented by the finding of HCV in PMBCs (Meller et al., 1993; Gunji et al., 1994; Cribier et al., 1995; Lerat et al., 1996) and bone marrow (Gabrielli et al., 1994). HCV has also been found at higher titer in lymph nodes than in sera from individual infected patients (Sugiyama et al., 1997), although it is not known whether this reflects replication and/or immune-based accumulation of HCV in vivo. The transmission of NANBH to a chimpanzee using PMBCs from a patient with NANBH implies that either HCV is transmitted passively upon transfer of the lymphoid cells or that these cells actually support replication (Hellings et al., 1985). The high frequency of HCV markers in selected lympho-proliferative disorders (Strassburg et al., 1996; Zignego & Brechot, 1999), in EMC (Gabrielli et al., 1994), and in nonHodgkin's lymphoma (Luppi et al., 1996) is also consistent with an etiologic role for HCV in these lymphoid diseases, although these correlative studies do not establish cause and effect. HCV replication has also been reported in primary biliary epithelial cells isolated from infected patients and in a gall bladder epithelial cell line (Ahmed et al., 1995; Loriot et al., 1999), although at the present time there is no known association between the infection of this cell type and biliary disease.