Tumorigenesis due to viral infection accounts for a high fraction of the total global cancer burden (15–20%) of all human cancers. One of the main mechanisms by which viruses induce host cell proliferation programs is through controlling the host’s epigenetic machinery. Oncogenic viruses establish a permanent latent infection sustained by the production of specific viral proteins, which interact with the cell environment, including the host epigenetic machinery to specifically deregulate pathways to their advantage such as cell metabolism, resistance to apoptosis, cell proliferation and innate immune response signaling. Epigenetic modifications largely alter host gene expression and can provide a common mechanism of virus-induced transformation.