Epidemiology of virus infection and human cancer

Based on the comprehensive assessment of epidemiological and mechanistic study findings, the International Agency for Research on Cancer has classified Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), Kaposi's sarcoma herpes virus (KSHV), human immunodefi ciency virus, type-1 (HIV-1), human T-cell lymphotrophic virus, type-1 (HTLV-1), and human papillomavirus (HPV) as Group 1 human carcinogens. The Merkel cell polyomavirus has recently been documented to cause Merkel cell carcinoma. No causal specifi city is observed for many oncogenic viruses. Some of them may cause different cancers, while some cancers may be caused by different viruses. However, only a proportion of infected persons will actually develop cancers, indicating that oncogenic viruses may be necessary but not suffi cient to cause specifi c cancers. Viral, host and environmental cofactors have been assessed for the EBV-associated nasopharyngeal carcinoma, HBV/HCV-associated hepatocellular carcinoma and HPV-associated cervical carcinoma. Persistent infection, high viral load, and genetic/acquired susceptibility factors are important risk predictors for these virus-caused cancers. Risk calculators have been developed for the prediction of the long-term risk of hepatocellular carcinoma among patients affected with chronic hepatitis B and C. Both clinical trials and national programs of immunization or anti-viral therapy have demonstrated a significant reduction in the incidence of cancers caused by HBV, HCV and HPV. Assessing the effects of gene-gene and gene-environment interactions on virus-caused cancers is urgently needed.