During infection with hepatitis B or C viruses, cytotoxic T lymphocytes (CTLs) have been implicated as both the mediators of protection and the principal effectors of liver pathology. Recent studies have allowed an investigation of the relationship between virus-specific CTL responses, liver damage and viral replication. In the presence of an efficient virus-specific CTL response, a scenario is emerging where inhibition of viral replication can be independent of liver pathology. We discuss the possibility that an inadequate CTL response--unable to control viral replication--may contribute to liver pathology not only directly but also via the recruitment of non-virus-specific T cells.