**1. Introduction**

Chronic hepatitis C virus (HCV) infection, together with chronic alcoholic liver disease, are the leading causes of hepatic cirrhosis and the development of hepatocarcinoma. Chronic HCV infection is the reason for about 50% of liver transplants in the western world; it is the second cause of liver transplants in northern Europe and and the main cause in countries such as Italy (Guillouche & Feray, 2011). In Spain, it accounts for 35% of all transplants (Registro Español de Trasplante Hepático [RETH], 2009). In fact, liver transplantation is currently the best therapeutic alternative for patients with advanced chronic liver disease due to HCV or those who develop hepatocarcinoma.

Reinfection of the graft is universal and occurs in 95% of patients transplanted due to HCV infection. This reinfection can compromise graft function and patient survival. In a few cases the histological recurrence is minimal and non progressive, though in most patients it follows a more rapid course than in immunocompetent persons, and frequently evolves to cirrhosis with graft loss. There also exists a pattern of recurrence which is very severe, but unusual (<10%) called fibrosing cholestatic hepatitis that often involves rapid graft loss (Roche & Samuel, 2010).

The elaboration of an efficient antiviral therapeutic strategy has been of paramount concern in clinical research in recent years, with questions about when, how much and at what point this treatment should be applied.

A considerable number of studies published over recent years have shown that antiviral treatment of post-transplant HCV hepatitis carried out during the late phase is the best option for improving the prognosis of these patients. Those patients who present a negative HCV serology after antiviral treatment have better survival (Picciotto et al, 2007).

The future perspectives concerning the introduction of new drugs for the treatment of chronic hepatitis C may involve therapeutic changes and, perhaps, a better prognosis for these patients.
