Hepatotropic viruses: new insights in pathogenesis and treatment

Hepatitis B virus (HBV) can be detected in peripheral blood mononuclear cells (PBMCs), mainly B lymphocytes and monocytes. The frequency of PBMC infection is higher in patients with ongoing HBV replication, but can persist for years after the complete resolution of an acute episode of hepatitis B. Infected PBMCs can act as reservoirs for the cell-to-cell transmission of the virus, and vertical transmission studies indicate that the HBV-infected PBMCs of mothers may act as a vector for intrauterine HBV infection. Recent data evaluated whether HBV occult infection could co-operate with HCV infection in the pathogenesis of mixed cryoglobulinemia (MC) and lymphoma and/or whether it may be implicated in the pathogenesis of MC and malignant diseases -B-cell non-Hodgkin's lymphoma (NHL) also independently from HCV. The treatment of chronic HBeAg-negative hepatitis B is intended to ensure the long-term suppression of HBV replication with the aim of halting the progression of liver damage and preventing the development of liver-related complications. This can be done by means of short-term "curative" treatment or long-term "suppressive" therapy. The first approach requires a 48-week course of peginterferon, which controls viral replication (HBV DNA <10.000 copies/ml) in 20-30% of patients; the second requires the long-term (possibly lifetime) administration of nucleoside and/or nucleotide analogues. As none of the currently available drugs alone suppresses viral replication (HBV DNA