Viruses have adopted many strategies to evade the immune response (Vossen et al., 2002). For example, many viruses down-regulate or inactivate the products of the major histocompatibility antigen class I locus to avoid immune clearance. In addition, herpesviruses such as EBV can enter latent states with limited viral gene expression to hide from the immune system (Klein, 1989). Nevertheless, virally transformed tumor cells often express viral proteins that can serve as tumor rejection antigens. Recognition of such neoantigens on virally induced cancer cells plays an important role in preventing viral tumorigenesis. Accordingly, immuno-suppression can permit the malignant proliferation of virally transformed cells that would be otherwise rejected. It is therefore not surprising that transplant recipients, congenitally immunodeficient persons, and AIDS patients are prone to develop EBV-carrying B-cell malignancies and other virally induced tumors including Kaposi sarcoma, and HPV-associated skin and cervical carcinomas (e.g., Beral et al., 1991). Strikingly, reconstitution of EBV-specific immunity can lead to regression of EBV-associated B-cell proliferations (Heslop et al., 1994; O'Reilly et al., 1997). These considerations suggest that manipulations that increase cellular immunity to viral antigens in cancer cells may be therapeutically useful.
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