The landscape of DNA virus associations across human cancers

The human cancer viruses have been found to cause 10-15% of all human malignancies. High-risk human papillomaviruses (HPV-16 and HPV-18), hepatitis B virus (HBV), and Epstein-Barr virus (EBV) contribute directly to cancer development, including cervical squamous cell cancer, hepatocellular carcinoma, Burkitt’s lymphoma, nasopharyngeal carcinoma, adult T cell leukemia, and Kaposi’s sarcoma. The roleof human cancer viruses in cancer pathogenesisis mediated through various mechanisms, including mutagenic integration into the host genome and expression of oncogenicviralproteins. The elucidation of such mechanisms has played a key role in enhancing our understanding of cancer pathogenesis even as novel aspects of DNA virus biology continueto be unraveled. In this chapter, we give aninsight of the main events responsible for the development of malignant tumors upon viral infection. With the availability of high-throughput sequencing and robust bioinformatics tools, it is possible to establisha landscape of viral integrationintohumancancer genome. Thus, we highlight the utility of RNA-Seq in detecting tumor-associatedDNA viruses and identifyingviral integration sites that mayunravel novel mechanisms of cancer pathogenesis. And we also describe a robust bioinformatics tool VirusSeq andits advantages in this field of study.