The causal associations between the seven viruses and specific cancers noted above are well established. They fulfill most, if not all, of the causality criteria proposed by Sir A. Bradford Hill in the early 1970s (Hill 1971). The strength and consistency of association between infection and cancer are high based upon multiple epidemiological studies in varying settings. For instance, the relative risk of HPV and KSHV infection for the development of cervical carcinoma and Kaposi’s sarcoma, respectively, is over 100 in most studies. In some instances, establishing a strong association required identification of especially oncogenic types, e.g., HPV16 and 18 among mucosotropic HPVs, and a specific subset tumors, e.g., oropharyngeal among head and neck cancers. Temporality was established by demonstrating that infection proceeded cancer, usually by many years. In some cases, the viruses are consistently detected in well-established cancer precursor lesions, as is the case for HPV and high-grade cervical intraepithelial neoplasia (Chap.​ 8). Dose–response relationships were established by demonstrating that, for the most part, populations with higher prevalences of virus infection also had higher incidences of the associated tumor, e.g., HBV and liver cancer (El-Serag 2012) (Chap.​ 5). However, these associations were sometimes confounded by high prevalence of the oncovirus in the general population and variability in the prevalence of additional risk factors. An example is the high frequency of EBV infection in the general population and the strongly associated cofactor of malaria infection in the induction of EBV-positive Burkitt’s lymphoma (Magrath 2012) (Chap.​ 10). Biological plausibility as oncogenic agents was established in numerous laboratory studies that identified the interaction of viral proteins with key regulators of proliferation and apoptosis, their immortalizing and transforming activity in vitro, and their oncogenic activity in animal models (Chaps.​ 4, 6, 8, 10, 11, and 13). These studies also support the criterion that the associations be in agreement with current understanding of disease pathogenesis, in this case, the process of tumorigenic progression. The last criterion, that removing the exposure prevents the disease, has been most convincing demonstrated for HBV, as discussed below and in Chap.​ 5.