One exception is a rare EBV-associated lymphoproliferative disease, which can occur shortly after infection. Viral cancers do not arise acutely after infection, but instead develop 15–40 years later. Oncogenic RNA viruses include, hepatitis C virus (HCV) and human T-cell lymphotropic virus-1 (HTLV-1). Oncogenic DNA viruses include EBV, hepatitis B virus (HBV), human papillomavirus (HPV), human herpesvirus-8 (HHV-8), and Merkel cell polyomavirus (MCPyV). Direct carcinogenic viruses possess viral oncogenes that directly contribute to neoplastic cellular transformation, whereas indirect carcinogens cause chronic inflammation, which can lead to oncogenic transformation. Oncoviruses are classified as direct or indirect carcinogens, although some overlap exists between the distinctions. Additionally, viruses are only an absolute requirement for oncogenesis in Kaposi sarcoma and cervical cancer. One or more additional insults, such as chronic inflammation, environmental mutagens, or immunosuppression, are required for cancer development. Oncovirus infections are common, but these infections rarely result in cancer. 80% of viral cancers occur in the developing world. Approximately 20% of all cancers are associated with infectious agents, and 12% of all cancers are caused by oncoviruses. Viral oncology knowledge and cancer surveillance have grown immensely since then. This finding built upon the landmark avian cancer virus research performed by Rous in the early 20th century. In 1964, the first human oncovirus was discovered, when Epstein-Barr virus (EBV) was detected in Burkitt lymphoma cells by electron microscopy.
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